OB-GYN

PLATI
F
NUM
IR S T E
FIRST D IT IO N
EDITION
2021
 ~
(
~)JOB-GYN
PLATINUM
-· . F I R S. lr E D I T I O N
2021

JERICHO THADDEUS P. LUNA, MD

ENRICO GIL C. OBLEPIAS, MD
CHRISTOPHER JOSEPH L. SORIANO, MD
NINA KATRINA C. BANZUELA-CRUZ, MD
PATRICIA ANN A. FACTOR, MD
JAIME ALFONSO M. AH ERRERA, MD
MARC DENVER A. TIONGSON, MD
ENRICO PAOLO C. BANZUELA, MD

EDITOR
LILIA P. LUNA, MD
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II
 NOTICE
The information in this book has been reviewed and verified with
reliable sources, and the approaches to management have been utilized
in clinical practice. However, medicine is an ever-changing science. New
research, changes in guidelines, and human error occur. The authors,
editor, and publisher are not responsible for errors or omissions or
for any untoward outcomes from application of data in this book. The
authors, editm; publisher, and other parties who have been involved in
the preparation of this book make no warranty, expressed or implied,
with respect to the completeness, accuracy, or being up-to-date of all
the information contained in this publication. The authors, editor, and
publisher encourage the readers to confirm the information herein
with other sources, and to exercise critical thinking based on the clinical
presentation of the patient in making decisions for management.

V
PREFACE
As a young medical student, I remember wishing that our textbooks were a
lot smaller and lighter than what they were back then. Having them available
at our fingertips at any time and anywhere for a quick review before an
exam, or before going on duty or attending a conference, would have been
convenient. Having an abridged consolidation of all our reference books is
just what we needed. With the Platinum series, students will have just that.
These reference manuals do not intend to replace the textbooks prescribed
by the medical curriculum. They are meant to be a reinforcement. The
Platinum series of books aims to allow medical students to correlate what
they encounter in the clinics and in the wards real time with the handy
features the books offer. The OBGYNPlatinum Team labored to give the
students access to answers to often asked questions of the specialty, from
the long-established prerequisite basic knowledge to the latest in clinical
practice guidelines. It is our prayer that, with this book, studying Obstetrics
and Gynecology would not be any more daunting to our students than it
should be.

Ricky 0.

VI
ACKNOWLEDGEMENT
To the Lord Almighty, who makes all things possible;

To our families, for their unfailing love and support: Capt. Jaime Julian & Mrs. Ma. Rosario
Aherrera; Dr. Gil Oblepias and Mrs. Ceny Oblepias, Dr. Corito Oblepias and children, Ed, Jics,
and Kori; Mrs. Yolanda Factor, Atty. Claire Factor, Mr. john Paul Factor, Mrs. Joanna Factor,
Mstrs. Cedric and Joaquin Factor, and Mr. Raffy Taruc; Mrs. Maria Cristina Tiongson, Dr. Lalaine,
Mstr. Matthew Damian Tiongson, Atty. Virgilio, Mrs. Marilyn, Ml'. Patrick Jeanne & Ms. Patricia
Meryl Tiongson, & Mr. Dennis, Mrs. Maita, Ms. Maiden Kristine & Mr. Andrei Nikolai Tiongson;
Mr. Jose R. Soriano, Jr. and Mrs. Nelly Soriano+, Emilio Joaquin, Justino Gabriel & Lucio Nicolas
Soriano, and Samantha Dominique, Angela Katrina & Nathan Soriano Onglatco; and Mrs. Arabella
Chiong-Banzuela, Ml'.Zeus Banzuela, Ms. Angelita Chiong, Mr. Nelson Cruz, Mrs. Epifania Cruz,
Attorney Napoleon Banzuela Jr., Dr. Rocky Lim & Ms. Arabella Aurora "Bogie" Lim Banzuela;

To our patients, especially the Filipino Patients - our greatest teachers, to whom the essence and
soul of this book is rooted on. This book is for you first and foremost;

To our mentors Dr. John Aiionuevo, Dr. Felix Eduardo Punzalan, Dr. Eric Oliver Sison, Dr. Jose
Fernando Fontanilla, Dr. Maria Luz Querubin, Dr. Judy Fuentes, Dr. Rowena Rivera, Dr. Marlyn
David-Ruaro+, Dr.Ferdinand Francis Cid, Dr. Maria Concellene Laforteza, Dr. Erlyn Sana, Dr. Alvin
Mojica, Dr. Robert Arias, Dr. Rose Ann Banal, Professor jenny Zapf, Professor Bobbi Kurshan,
Mr. Jojo Fresnedi, Mrs. Rhodora Palomar-Fresnedi, Dr. Ramon Paterno, Dr. Rommel Duenas, Dr.
Pacifico Eric Calderon, Dr. Eric Calderon Jr., Dr. Mark Louie Mann for their invaluable guidance
and wisdom;

To Dr. Florante Gonzaga, Dr. Rosalinda Arceo, Dr. Lyra Ruth Clemente-Chua and DI'. Greg
Pastorfide (Reproductive Endocrinology and Infertility]; Dr. Blanca De Guia - Fuerte (Pediatric
and Adolescent Gynecology); Dr. Virgilio Oblepias, Dr. Felix Salgado, and Dr. Azucena Suplido
(Minimally Invasive Surgery, Mullerian Anomalies, and Family Planning) for having planted in us
the love and interest for Reproductive Medicine;

To our colleagues and mentors from Asian Hospital & Medical Center; FEU-NRMF Department
of Obstetrics and Gynecology, Institute for Women's Health, The Medical City, and UP-Philippine
General Hospital, especially the Department of Obstetrics and Gynecology, Division of
Reproductive Endocrinology and Infertility, Division of Family Planning;

To our colleagues, fellow teachers and bosses from San Beda University College of Medicine,
Ateneo School of Medicine and Public Health, De La Salle Medical and Health Science Institute,
Bicol University College of Medicine, and New Era University College of Medicine for enabling us
to undertake this endeavor;

To all main authors, contributing writers of the IM Platinum, Surgery Platinum, Pedia Platinum
and Philippine Medical Jurisprudence, thank you very much for all your help in making the
Platinum Series Dream come true;

To the Phi Kappa Mu Fraternity;

To the Philippine Society of Physiologists;

To All the Teachers, Mother Geese, Mentors and Staff of Topnotch Medical Board Prep;

To Cohort 5 of the University of Pennsylvania Masters in Educational Entrepreneurship.

Classmates from Asian Institute of Management MDP Batch 97, University of Oxford Department
of Continuing Education and Maastricht University MHPE

To Our Dearest Students, our reason for being.

This book is lovingly dedicated to Atty. Virgilio Tiongson t, Mr Constantino Luis G. Factor Ill t,
and Denver's three little angels in heaven.

Ricky L., Ricky 0., Chris, Nifia, Patty, Jaime, Denver, and Broli

VII
 For all the medical students,
may this OB-GYN Platinum book
help you in your rotation and exams
in Obstetrics and Gynecology.

Ricky L.

VIII
 AUTHORS
THE
Jericho Thaddeus P. Luna, MD, FPOGS, FSGOP, FPSCPC
Dr. Luna is a graduate of the University of the Philippines College of Medicine (UPCM), Manila Class ofl 993 and a member
of the UPCM Phi Kappa Mu Fraternity. He has completed a 4-year residency training in Obstetrics and Gynecology
and a 3-year fellowship training in Gynecologic Oncology at the Philippine General Hospital (PGH), University of the
Philippines, Manila. Since 2001, he has been a member of the Faculty of the Department of Obstetrics and Gynecology,
UPCM where he is now a Professor 12 and the current Chief of the Division of Gynecologic Oncology. He is a Fellow of
the Philippine Obstetrical and Gynecological Society (POGS), the Society of Gynecologic Oncologists of the Philippines
(SGOP) and the Philippine Society of Cervical Pathology and Colposcopy (PSCPC). Aside from the POGS, SGOP & PSCPC,
Dr. Luna is also a member of the following Societies: Asia Oceania (research organization on) Genital Infections and
Neoplasia-Philippines [AOGIN Phils.], Philippine Society of Climacteric Medicine (PSCM), Philippine Society of Fertility
Preservation (PSFP), Philippine Society of Oncology, University of the Philippines-Manila Medical Alumni Society
(UPMAS), European Society of Gynaecological Oncology (ESGO) and International Gynecological Cancer Society (IGCS).
He has served as President in the following Societies: AOGIN-Phils. (2015-2016), UPMAS (2018), SGOP (2019) & PSCM
(2019-2020). He has been a member of the POGS Board of Trustees (BOT) where he served as Treasurer (2010-2012,
2016-2017) and Chair of both the Committees on Clinical Practice Guidelines and Scientific Works (Research) in 2015.
He has been the Editor-in-Chief of the Philippine Journal of Obstetrics and Gynecology (PJOG) since 2014. He is a
current Board Member of the PSFP and the PGH Alumni Association of the Department of Obstetrics and Gynecology
(AADOG). He has been the recipient of the following awards: Asia Oceania Federation of Obstetrics and Gynecology
(AOFOG) Young Gynaecologist Award (2002), PGH lntern's Award for Best Consultant (2002), UPCM Outstanding
Faculty in the Clinical Sciences (2005), POGS Young Researcher Award (2005), Department of Science and Technology-
National Academy of Science and Technology (DOST-NAST) Outstanding Young Scientist (2006), PSO Outstanding
Cancer Researcher Award (2010), UP Manila Gawad Chancellor Outstanding Researcher Award (2010), Metrobank
Foundation Outstanding Teacher (2011), Philippine National Health Research System (PNHRS) Best Mentor in Health
Research Award (2011), UPCM Best Teacher in the Clinical Department - LU 6 (AY 2011-2012), Philippine Medical
Association (PMA) Dr. Jose P. Rizal Memorial Award for Research (2017), POGS Honoria Acosta-Sison Award of Merit for
Research (2018) and the UP Manila Gawad Sentenaryo Professorial Chair Award in recognition of exemplary training,
service and teaching performance in Gynecologic Oncology (2019). Aside from being a known teacher, researcher and
gynecologic surgeon, Dr. Luna enjoys organizing continuing medical education (CME) activities, conducting gynecologic
surgery & cervical cancer screening workshops and missions, traveling (local and abroad), driving & going on road
trips, watching movies and gathering Starbucks collectibles.

Enrico Gil C. Oblepias, MD, FPOGS, FPSRM, FPSGE

Dr. Oblepias graduated from the University of the Philippines - College of Medicine (UPCM), Pedro Gil. Manila in
1989. He took and completed his residency training in Obstetrics & Gynecology in the Philippine General Hospital,
Taft Avenue, Manila in 1993. He moved on to finish a fellowship training program in Reproductive Endocrinology
and Infertility at the same institution in 1995. In 1997, he joined the faculty of UPCM where he is now Professor 8
and currently the Chief of the Department of Obstetrics and Gynecology's Division of Reproductive Medicine. He was
also the department's Vice-Chair for Research from 2009 - 2012. He is a member of the Phi Kappa Mu Fraternity and
served as Faculty Adviser to the Fraternity from 2016-2017. He was President of the Philippine Society of Reproductive
Endocrinology and Infertility (PSREI), now the Philippine Society of Reproductive Medicine (PSRM), in 2011. Over
the years he has been a recurrent member of the Philippine Obstetrical and Gynecological Society's (POGS) Board of
Trustees where he served as Public Relations Officer in 2017, and chaired at different times the Committee on Scientific
Works (Research), Committee on Clinical Practice Guidelines, Committee on Hospital Accreditation, Committee on
Nationwide Statistics, and Committee on Community Service. Apart from being a published author in journals and
in books, he was co-editor of the POGS Research Handbook, and has also been a member of the editorial board of the
Philippine Journal of Obstetrics and Gynecology, the Philippine Journal of Reproductive Endocrinology and Infertility,
and the Philippine Journal of Pediatric and Adolescent Gynecology. Aside from the medical societies already mentioned,
he is also a member of the following subspecialty societies: the Philippine Society for Gynecologic Endoscopy (PSGE);
the Pediatric and Adolescent Gynecologic Society of the Philippines (PAGSPHIL); the Philippine Society for Climacteric
Medicine (PSCM); the Philippine Society for Fertility Preservation (PSFP); and the Philippine Society for Responsible
Parenthood (also known as the Philippine Family Planning Society). Dr. Oblepias has been the recipient of the following
awards: the UP-Manila Centennial Faculty Grant (UP Manila) in 2009; the Dr. Augusto Manalo Professorial Chair (UP
Manila) in 2020; the Leadership Award (Bayside Council in Obstetrics and Gynecology or BAYCOG)in 2013; and the
Honoria Acosta-Sison Award of Merit for Research (POGS) in 2014. Dr. Oblepias is a devoted husband and father. As a
hobby, he collects Star Wars memorabilia and toys.

Christopher Joseph L. Soriano, MD, MHPEd, FPOGS

Dr. Soriano graduated with a S.S. Psychology degree, from UST College of Science in 1996. He obtained his medical
degree from UST Faculty of Medicine & Surgery in 2001. He was awarded the Most Outstanding Intern at Chinese
General Hospital in 2002. He completed his residency training in Obstetrics & Gynecology at The Medical City where
he was given the GEM (Going-the-Extra-Mile) Award: Most Commended Resident by the Patient's Assistance Office
in 2004. Because of his love for teaching, he obtained his Master's in Health Professions Education (MHPEd) at the
National Teacher Training Center for the Health Professions (NTTC-HP), UP Manila in 2016. He is currently a full-time,
assistant professor at the Ateneo de Manila School of Medicine and Public Health (ASMPH) where he serves as module
coordinator & subject expert in Obstetrics, student mentor and coach, and member of the research ethics committee.
He currently serves as Assistant Training Officer for 08-GYN residency training at The Medical City. He is also an active
member of the Task Force on Gender-based Violence of the Philippine Obstetrical & Gynecological Society. He provides
public service on-air as regular host of Doctors-on-Line at 702 DZAS.Chris loves running as a sport and has ran several
marathons. He also likes swimming, travelling, and nature & food tripping.

IX
Nifi.a Katrina C. Banzuela-Cruz, MD, MHPEd, FPOGS
Dr. Banzuela-Cruz is a woman of many hats. She finished her education in Biology at The Ateneo de Manila University
and proceeded to her Doctor of Medicine Degree in the Pamantasan ng Lungsod ng Maynila. She continued further
training as a 08-GYN in the Far Eastern University-Nicanor Reyes Medical Foundation. After graduating from her
residency training, she also pursued a career in education and continues to improve herself as an educator by taking up
a Masters in Health Professions Education at the University of the Philippines-National Teachers Training Center which
aided her in inspiring students through her 08-GYN lectures in Topnotch Medical Board Prep and Physiology lectures
in San Beda College of Medicine. She believes that competence and kindness are the ideal values that all doctors should
have and these principles embody her as she continues to inspire and guide students as the head of the Mentoring
Program of Topnotch Medical Board Prep. She enjoys good food with good company. Her heft and height partnered
with her joyous laughter makes her stand out from a crowd. These traits serve as endearing qualities that makes her
well-loved by her patients, colleagues and students. Her family serves as her ultimate inspiration.

Patricia Ann A. Factor, MD, DPOGS, FPSRM

Dr. Factor graduated with a B.S. Biology degree, cum laude, from UP Manila in 2007. She obtained her medical
degree from the UP College of Medicine in 2012. Patty finished her residency in Obstetrics and Gynecology at the UP-
Philippine General Hospital. where she served as Assistant Chief Resident in her senior year. She pursued a fellowship
in Reproductive Endocrinology and Infertility at the Philippine General Hospital and was the Chief Fellow for the
Department of Obstetrics and Gynecology in 2019. Throughout her training, she presented numerous papers at both
national and international conventions. Patty is part of the clinical faculty of the Division of Family Planning of the
Department of Obstetrics and Gynecology of the UP-PGH. She is currently enrolled in the Masters in Epidemiology
(Clinical Epidemiology) at the UP College of Medicine. Her research interests include: infertility, endometriosis, and
menopause. In her spare time, Patty enjoys lazy days at the beach, traveling, and cooking.

Jaime Alfonso M. Aherrera, MD, FAMP, FPCP, FPCC

Dr. Aherrera graduated with a B.S. Human Biology degree from De La Salle University-Manila and obtained his medical
degree from the De La Salle University-Health Sciences Institute, garnering awards including the Dean's Special Award
for Academic Performance and Special Citation for Academic Excellence. He was also a board topnotcher during the
Philippine Physician Licensure Examinations in August 2009. He completed his residency training in Internal Medicine
and fellowship in Cardiology and lnterventional Cardiology at the University of the Philippines - Philippine General
Hospital (UP-PGH). where he was Chief Fellow and recipient of both the Dr. Ramon Abarquez Most Outstanding Fellow
Award and the Dr. Clemente Gatmaitan Most Outstanding Fellow in Research Award. He is currently completing his
Masters Degree in Clinical Epidemiology at the UP-Manila College of Medicine. At a young age, he has already completed
an impressive portfolio, including four editions of IM Platinum, which was awarded as one of the Outstanding Books of
2016 by the National Academy of Science and Technology (NAST). He was also winner of the prestigious Dr. Francisco
Tangco Young Investigator's Award from the Philippine Heart Association for two consecutive years (2014 and 2015),
recipient of the Most Outstanding Fellow in Cardiology of the Philippine Heart Association in 2016, and topnotcher of
the Cardiology Diplomate Examination that same year. Recently, he was awarded as an Outstanding Young Scientist by
the NAST in 2020. He is a Fellow of both the Philippine College of Physicians and the Philippine College of Cardiology,
a Member of the Philippine Society of Cardiac Catheterization and Interventions, and is presently practicing as an
lnterventional Cardiologist at the Asian Hospital Medical Center, UP-PGH, Manila Doctors Hospital, and Medical Center
Manila. Despite these sterling achievements, Jaime remains grounded, down to earth, and a jolly friend to his peers
and colleagues.

Marc Denver A. Tiongson, MD, FPCP, FPCC

Dr. Tiongson graduated with a Bachelor in Science in Biology, major in Cell and Molecular Biology, cum laude, from
the University of the Philippines-Los Banos in 2006. He pursued on to obtain his medical degree from the UP College
of Medicine in 2011 and was awarded outstanding intern in several clinical departments. Upon passing the medical
board exams, he became a faculty member of the San Beda College of Medicine and Topnotch Medical Board Prep
teaching Physiology, Biochemistry, Anatomy, Pharmacology and Pathology. Shortly after, he trained and completed his
residency in Internal Medicine at the Philippine General Hospital in 2015, during which he served as the Assistant Chief
Resident for Information Management System. He finished his Cardiology Fellowship and lnterventional Cardiology
Fellowship at the same hospital where he served as both the Chief Fellow for the Division of Cardiovascular Medicine
and Overall Chief Fellow for the Department. His interest in research garnered him awards in local and international
conferences. On top of this, he was able to publish his works in highly regarded scientific journals. He likewise co-
authored IM Platinum, Pedia Platinum, and Surgery Platinum. Because of his extraordinary achievements he was
awarded the Dr. Ramon F. Abarquez Most Outstanding Fellow, Dr. Celemente Gatrnaitan Most Outstanding Fellow in
Research, and Philippine Heart Association Most Outstanding Training Fellow in Cardiology for 2019. He is a Fellow
of both the Philippine College of Physicians and the Philippine College of Cardiology. He also held the position as the
national representative of the Philippines to the Heart Failure Association of the European Society of Cardiology - Heart
Failure Specialists of Tomorrow from 2018 to 2021. Currently, he is the Vice President of Topnotch Medical Board Prep
and also practices as an lnterventional Cardiologist. Despite his seemingly busy schedule, Denver remains to be a well-
rounded guy and a proud family man who values time with his family especially his wife, Lalaine and son, Matthew; and
friends. His interests span video games, watching movies and binging on Netflix.

X
Enrico Paolo C. Banzuela, MD, MSEd, MHPEd, FPSP
Dr. Banzuela graduated with a 8.S. Basic Medical Sciences degree (INTARMED) from UP Manila in 2002. He obtained
his medical degree from the UP College of Medicine in ZOOS.He finished his Masters in Educational Entrepreneurship
(MSEd) at the University of Pennsylvania in 2019. He obtained his Diploma in Health Professions Education from
the UP National Teacher Training Center for the Health Professions in 2018. He also a graduate of the Management
Development Program of the Asian Institute of Management in 2018. He also has a Postgraduate Certificate in Teaching
Evidence-Based Health Care at the University of Oxford in the United Kingdom in 2020. He is currently taking a Masters
in Health Professions Education (MHPE) at the University of Maastricht in the Netherlands. Upon passing the medical
board exams in 2005, he served as a volunteer physician for the 2005 Manila Southeast Asian Games. He also worked as
a University Researcher for the UP National Institutes of Health under the Phil Health Research Study Group for 3 years.
He co•authored a book entitled "Survival Guide for Doctors (and Non·Doctors Too) with Dr. Willie Ong and D1:Liza Ong.
He is also a co-author of IM Platinum, Surgery Platinum, Pedia Platinum and now, Ob-Gyn Plaltinum. Dr.Banzuela is the
Chair of the Section of Medical Physiology (Associate Professor II) at the San Beda University College of Medicine and
has been a faculty member since 2005. he has also served previously as lecturer for Biochemisty, Neurology, Family and
Community Medicine at the same institution. He is guest lecturer for Biochemistry at the Ateneo School of Medicine
and Public Health. He currently serves as Vice-President of the Philippine Society of Physiologists. He is the President of
Topnotch Medical Board Prep where he also teaches Physiology. Dr.Banzuela has always been involved with preparing
doctors for the medical board exams since 2005, having written guides, given orientation talks, created school•specific
board exam programs and lectured subjects at various hospitals and institutions. He enjoys fishing, driving, playing
basketball, listening to vinyl records, perfecting his aquaponic setup and going on food trips with his family.

THE
EDITOR
Lilia P. Luna, MD, FPOGS
Dr. Lilia P. Luna is a cum laude graduate of FEU-NRMF Institute of Medicine and one of the 10 topnotchers in the Philippine
Medical Board Examination in 1961. She had her residency training in OBGYNat FEU Hospital, and had her fellowship in
Reproductive Infertility and Menopause (RM) at the New York University Medical Center and a postgraduate course in Family
Planning at the University of Colorado. After her fellowship, she joined the consultant staff and faculty of FEU-NRMF.She
became the chairman of the Department of OB-GYNof United Doctors Medical Center and Capitol Medical Center. She has a
degree in Master in Hospital Administration from the Institute of Public Health of the University of the Philippines. She was
appointed Chief of Clinics, and subsequently, Hospital Director of FEU-NRMF Hospital for 18 years. She was instrumental
(together with FEU-NRMF alumni) in the putting up of the Marian Medical Arts Bldg AND Marian Radiology Cente1~near
FEU-NRMF Medical Center. She established a 2-year fellowship program in Reproductive Medicine, a Consortium between
FEU-NRMF Hospital, Jose Reyes Memorial Medical Center, and Capitol Medical Center. To date, this fellowship program has
graduated 20 fellows, who have all been certified by the Phil, Board of Reproductive Medicine and some, by the Phil. Society of
Gynecologic Endoscopy. She is currently on her 55th year as faculty member of FEU-NRMF and is still very active in practice
and in training OB-GYNresidents and fellows in Reproductive Medicine.

Her expertise in OB-GYNpractice and in Reproductive Medicine is well recognized, both by her very busy OGYNpractice, as
well as her colleagues. She assumed several positions in the Philippine OB-GYNSociety, such as Treasurer, Editor in Chief,
POGS Journal, member of the Board of Trustees, Chairman of various committees, Vice-President, and President (1991 ). She
also was ve1y active in and subsequently became President of the Phil. Society of Climacteric Medicine and Phil. Society
Of Reproductive Medicine. Up to the present, she is member of the Credentialling Committee of the Philippine Society of
Gynecologic Endoscopy. She is a member of the POGS Committee on Ethics AND PSRM Credentials and Ethics committees.
She has numerous publications in scientific manuals, books, and clinical practice guidelines of POGS,and Specialty Societies.

In recognition of her expertise in obstetrics & gynecology, she received the following awards: POGSBALDOMERORoxas Award
for Academic Excellence (2000), Honoria Acosta Award for Research (2006) and the Professional Regulations Commission
of the Philippines as Outstanding in the Field of Medicine. She was cited in the Reader's Digest as one of the Philippines'
Most Trusted in the Field of Medicine (2010). Internationally, she received the Woman of the Year Award from Federation
International Obstetrics & Gynecology (FIGO) in 2009. She received various awards as Outstanding Alumni of Far Eastern
University. FEU-NRMF Medical Foundation has awarded her the following: Most Outstanding Alumni, Most Outstanding
Faculty Member; Most Outstanding Leader, Most Outstanding in Clinical Practice.

She is currently professor emeritus and senior consultant in FEU-Nicanor Reyes Medical Foundation, Medical Director
and Senior Consultant of Capitol Medical Center. She continuously participate as lecturer or attendee in various scientific
programs /webinars of POGS,PSRM,PSCMAND PSGE.

XI
CONTRIBUTING
AUTHORS
Ira Dominique T. Alatraca-Malonzo, MD, FPOGS, FPSURPS
Dr. Alatraca-Malonzo was part of the Integrated Liberal Arts and Medicine (lntarmed) Program of the
University of the Philippines College of Medicine, graduating with a bachelor's degree in Basic Medical
Science in 2004 and Doctor of Medicine in 2009. She completed her residency training in Obstetrics &
Gynecology in 2013 at the UP Philippine General Hospital and proceeded with subspecialty training
in Urogynecology and Pelvic Reconstructive Surgery in the same institution, graduating in 2015.
While in training, she won in national interesting case and research competitions, with a few published scientific papers
under her belt. She continued to present her scientific works on Urogynecology in local and international fora and won
3rd place in the Young Urogynecologists Research Competition of the Asia-Pacific Urogynecology Association in 2017.
She then joined the faculty of the UPCM,serving as a clinical associate professor, and is presently the Assistant Training
Officer of the Division of Urogynecology and Pelvic Reconstructive Surgery of UP-PGH. She is a fellow of the Philippine
Obstetrical and Gynecological Society (POGS) and was a member of its Continuing Medical Education Committee
from 2018 to 2020. She is also a fellow and is the current secretary of the Philippine Society for Urogynecology and
Reconstructive Pelvic Surgery (PSURPS). She is also a Medical Specialist II at the Dr. Jose Fabella Memorial Hospital.
In 2019, Dr. Malonzo was conferred the Constantino P. Manahan Young Researcher Award by the POGS. In the same year,
she was also one of the Shan S. Ratnam Young Gynecologist Awardees of the Asia and Oceania Federation of Obstetrics
and Gynecology. Dr. Malonzo is wife to a software architect and manager and is the proud morn of a witty 9-year old boy.
She enjoys baking, growing orchids and dancing during her free time. She is also a strong supporter of Filipino designers
and artisans, and is particularly fond of handcrahed jewelry and accessories.

Ma. Gemma D. Fulgado, MD, FPOGS, FPSMFM

Dr. Fulgado graduated from FEU-NRMF Medical Center and pursued both her OBGYNresidency and fellowship training
in perinatology in the same institution. Currently, she is a clinical consultant of FEU-NRMF Medical Center and an active
OBGYN-High Risk Pregnancy Specialist in the Rizal Province. Our author has also been a contributor to a number of
Clinical Practice Guidelines of the POGS.

Zarinah G. Gonzaga, MD, FPOGS, FPSMFM, FPSUOG

Dr: Gonzaga graduated with a 8.S. in Community Nutrition at the University of the Philippines, Diliman. She obtained her
medical degree from the Faculty of Medicine and Surgery of the University of Sta Tomas in 2001. She had her residency
training in Obstetrics and Gynecology at The Medical City, Pasig where she served as the Chief Resident during her
senior year. Thereafter, she pursued fellowship training in Maternal-Fetal Medicine and in Ultrasound in Obstetrics
and Gynecology in the same institution. During her training, she has won several national research paper competitions
and presented in international scientific fora. She was the overall topnotcher of the subspecialty board written, oral
and practical examinations given by the Philippine Society of Maternal Fetal Medicine (PSMFM). She has served in the
PSMFM as a specialty board examiner in 2016 to 2017 and a training program accreditor in 2017. She was given the
Physician Leadership Award at The Medical City in 2018 for her service as the Assistant Chair of the Department of
Advanced Medical Education from 2014 to 2017. She is an Assistant Professor at the FEU-NRMF Institute of Medicine,
Clinical Faculty and Lecturer at the Ateneo School of Medicine and Public Health, and a member of the Faculty of the
Philippine Obstetrics and Gynecologic Society (POGS) first Online Review Course. She has served as the Section Head
of the Section of Maternal Fetal Medicine of the Institute for Women's Health of The Medical City since 2018 to present
and was awarded Best Mentor for the Section of Maternal Fetal Medicine for three consecutive years. Currently she is
the Assistant Treasurer of the Board of Trustees and the Chair of the Committee on Continuing Medical Education of
the Philippine Society of Maternal Fetal Medicine (PSMFM). She is currently finishing her double Master's degree in
Business Administration and Hospital Management. Rinah's professional advocacy include prenatal diagnosis of fetal
anomalies and preeclarnpsia prediction and prevention. Rinah is a proud morn of three teenagers and wife to a doting
husband. She loves travelling, reading and yoga.

Ma. Concellene L. Laforteza, MD, DPBA, MHPEd, FPSA

Dr Laforteza graduated with a BS Nursing degree from the University of Santo Tomas in 1980. She obtained her
medical degree from the Manila Central University then went on to specialize in Anesthesiology at the University of the
Philippines - Philippine General Hospital. She has been in clinical practice for 35 years and has served as chairperson
for the Department of Anaesthesiology at the Fe de! Mundo Medical Center (FD MMC,formerly Children's Medical Center
Philippines) where she currently holds the position as the hospital's Chairman for FDMMC's Pain Center. She is currently
one of the Directors of the Regional .~nesthesia Society of the Philippines. She served her specialty society in different
capacities before she became the Vice President of the Philippine Society of Anesthesiologists. She was appointed to be
part of the Professional Regulation Commission's (PRC's) Technical Working Group of Professional Medical Educators
as she also finished her Masters in Health Professions Education at the University of the Philippines, where she was
a College Scholar. She is also an academician connected with San Seda University as Head of the Office of Medical
Education's Faculty Development Unit. Because of her training and experience, she is often asked to serve as speaker
for various conventions and assemblies. She loves to travel with her ever supportive husband, who is a pediatrician,
and her daughter, who just finished her training in anesthesiology and now aspires to be like her anesthesiologist morn.

XII
Agnes L. Soriano-Estrella, MD, MHPEd, FPOGS, FPSSTD
Dr. Agnes L. Soriano-Estrella obtained her medical degree from the University of the Philippines College of Medicine.
She had her residency in Obstetrics and Gynecology and fellowship training in Trophoblastic Diseases at the Philippine
General Hospital. Soon after graduation, she joined the faculty of the Department of Obstetrics and Gynecology of
the College of Medicine of the University of the Philippines, Manila where she is currently an Associate Professor and
training officer of the Division ofTrophoblastic Diseases. She obtained a Masters degree in Health Professions Education
from the National Teacher Training Center for the Health Professions of the University of the Philippines, Manila. Dr.
Soriano•Estrella is a founding member and the current President of the Philippine Society for the Study ofTrophoblastic
Diseases. She has authored several articles on general obstetrics and gynecology as well as trophoblastic diseases,
which have been published in national and international peer reviewed journals. She was the editor of the Clinical
Practice Guidelines for the Diagnosis and Management ofTrophoblastic Diseases published in 2016 and the Associate
Editor of the Handbook of Trophoblastic Diseases published in 2012. She is likewise one of the editors of the Atlas
of Trophoblastic Diseases which garnered a Book Award from the National Academy of Science and Technology. She
has also authored chapters in several books and has been a member of technical committees for some clinical practice
guidelines published by the Philippine Obstetrical and Gynecological Society. In recognition of her work in the field of
Research, she was given the Most Outstanding Young Researcher Award by the Philippine Obstetrical and Gynecological
Society in 2009

Florida F. Taladtad, MD, FPOGS, FPIDSOG

Dr. Florida F.Taladtad is a graduate of the INTARMED program of the University of the Philippines, Manila College of
Medicine (UPCM) Class 2011. She completed her Residency training in the Department of Obstetrics and Gynecology
of the Philippine General Hospital (PGH) last 2015. She finished her fellowship training on Obstetric and Gynecologic
Infectious Diseases at the UP-PGH, last December 2018. She is a Fellow of the Philippine Obstetrical and Gynecological
Society (POGS) and a Fellow of the Philippine Infectious Diseases Society for Obstetrics and Gynecology (PIDSOG).
Dr. Taladtad is an Associate Professor 2 of the UPCM Department of Anatomy and is also a Faculty of the Division of
Infectious Diseases, Department of Obstetrics and Gynecology, UP·PGH. She is a Medical Specialist 2 at the Jose B. Lingad
Memorial General Hospital (JBLMGH). She has co·authored several published researches during her training, and is a
contributing author and editor of handbooks and COVID-19 guidelines published by POGS & PIDSOG.

CONTRIBUTING
WRITER
FORBOARD
CORRELATES
AND
LAYOUT
EDITOR
Manuel S. Vidal, Jr., RCh, MD
Dr. Vidal graduated with a BS Biochemistry degree, magna cum laude, from the De La Salle University- Manila under the
Star Scholarship Program, with several other awards: Excellence in Chemistry, Most Outstanding Thesis, and Dr.Jose Rizal
Honors Society inductee. He ranked second in the Chemistry Licensure Examination in 2014. He finished his medical studies
at the University of the Philippines Manila - College of Medicine, and is about to embark on his PhD dissertation studies
on organ-on·chip models at the University of Texas Medical Branch, Galveston, Texas. He dreams on becoming a good
OB·GYN in the future. If not busy, he enjoys the laid-back life, collecting fragrances, sipping coffee, drinking beers, and
cooking wonderful food for his friends. He is thankful for the opportunity to work on the first edition of this book.

ILLUSTRATORS
Christian Paolo S. Vidal, RMT
Mr. Vidal is a licensed medical technologist, graduating from the University of the Philippines Manila - College of
Public Health. He is currently undertaking his Master's degree in Public Health at the same institution under the DOST·
ASTHRDP scholarship program. He is a recipient of the University of the Philippines International Publication Award in
2020. At present, he works as a teaching associate at the College of Public Health, University oFthe Philippines Manila.
He is thankful for the invitation to contribute to the Platinum book series.

Manuel S. Vidal, Jr., RCh, MD

XIII
TABLE
OFCONTENTS
1:ANATOMY
CHAPTER ANDPHYSIOLOGY
OFTHE
FEMALE
REPRODUCTIVE
SYSTEM
Section 1: Anatomy of the Female Reproductive Tract
Anatomy of the Female Reproductive System
External Genitalia 4
Internal Genitalia 6
Ureters 10
General Blood Supply of the Female Reproductive System 10
The Female Pelvis II
Diaphragm and Ligaments 13
Clinical Correlates 14
Section 2: The Menstrual Cycle 15
Review of the Hypothalamic-Pituitary-Ovarian (HPO) Axis 15
Overview of the Menstrual Cycle 16
Section 3: Maternal Adaptations to Pregnancy 21
Reproductive Tract 21
Breast and Skin 22
Metabolic Changes 23
Hematologic System 24
Cardiovascular System 25
Pulmonary System 26
Urinary System 28
Gastrointestinal System 29
Endocrine System 30
Neuromuscular System 31
The Placenta and the Umbilical Cord 32
Section 4: Fetal Development 33
Fetal Development 33
Amniotic Fluid 35

CHAPTER
2:APPROACH
TOTHE
PATIENT
INOBSTETRICS
Section 1: Overview 39
Definition of Terms 39
Diagnosis of Pregnancy 41
Pregnancy Tests 42
Section 2: Preconceptional Care 44
Overview of Preconceptional Care 44
Components of Preconceptional Care 44
Section 3: Prenatal Care 49
Overview of Prenatal Care 49
Initial Prenatal Evaluation SI
Prenatal Surveillance 57
Dating of Pregnancy 58
Nutritional Counseling in Pregnancy 61
Common Concerns 65
Immunization for Filipino Pregnant Women 66
Section 4: Antenatal Surveillance 68
Overview of Antepartum Fetal Surveillance 68
Non•stress Test 68
Contraction Stress Test 69
Umbilical Artery Doppler Velocimetry 69
Biophysical Profile (BPP) 70

CHAPTER
3:LABOR
ANDDELIVERY
Section 1: Mechanism of Labor 75
Section 2: Physiology of Labor 91
Preparation for Labor 91
Phases of Parturition or Labor 91
Functional Divisions (Stages) of Labor 93
Section 3: lntrapartum Assessment 100
Electronic Fetal Heart Rate Monitoring 100
Baseline Fetal Heart Activity 101
Periodic Fetal Heart Rate Changes 102
Three•tier Fetal Heart Rate Interpretation 106
Section 4: Induction of Labor 107
Section 5: Management of Labor in the Vertex Position 109
Management of the First Stage of Labor 109
Management of the Second Stage of Labor 113
Management of the Third Stage of Labor 115
Management of the Fourth Stage of Labor 118

XIV
TABLE
OFCONTENTS
CHAPTER
4:DYSTOCIA
[ABNORMAL
LABORJ
Section 1: Mechanisms ofDystocia 121
Review of Normal Labor 121
Dystocia ("Difficult Labor") 124
Diagnosis of Abnormal Labor 125
Section 2: Sepcific Causes ofDystocia 126
"Power" (Uterus) 126
"Passenger" (Fetus) 128
"Passage" (Pelvis of Mother) 133

CHAPTER
5:PROCEDURES
INOBSTETRICS
Section 1: Instruments Used in Obstetrics and Gynecology 137
Section 2: Operative Vaginal Delivery 145
Forceps Delivery 145
Vacuum Assisted Delivery 148
Section 3: Breech Delivery 150
Section 4: Cesarean Section (CS) and Vaginal Birth After CS 156
Cesarean Section 156
Vaginal Birth After Cesarean 159
Section 5: Obstetric Analgesia and Anesthesia 160
Regional Anesthesia 160
General Anesthesia 163

CHAPTER
6:PUERPERIUM
Section 1: The Puerperium 167
The Puerperium (Postpartum Period) 167
Maternal Changes During the Puerperium 167
Postpartum Care 171
Section 2: Postpartum Complications 172
Postpartum Hemorrhage 172
Puerperal Complications 174
Thromboembolic Disease 177
Uterine Complications in the Puerperium 178
Disorders of the Breast 179
Other Problems in the Puerperium 180
Section 3: Breastfeeding and Lactation 181

CHAPTER
7:BLEEDING
DURING
PREGNANCY
AND
INPOSTPARTUM
Section 1: Overview of Bleeding During Pregnancy 187
Section 2: Early Pregnancy Complications 188
Abortion 188
Ectopic Pregnancy 192
Section 3: Bleeding in the Second Half of Pregnancy 199
Placenta Previa 199
Abruptio Placenta 20 I
Morbidly Adherent Placenta (Accrete Syndromes) 205
Disseminated lntravascular Coagulation (DIC) 207
Section 4: Postpartum Hemorrhage 212
Uterine Atony 212
Retained Placenta or Placental Fragments 214
Uterine Rupture 215
Uterine Inversion 217
Genital Tract Trauma 220

CHAPTER
8:GENERAL
OBSTETRIC
ISSUES
ANDCOMPLICATIONS
Section l: Preterm Labor 227
Prelabor Rupture of Membranes 235
lntraamniotic Infection and Chorioamnionitis 237
Section 2: Fetal Demise, Postterm Pregnancy, and Prolapsed Cord 238
Section 3: Multiple Gestations 244
Section 4: Fetal Growth Disorders 248
Fetal Growth Restriction 248
Fetal Macrosomia 250
Section 5: Abnnormalities in Amniotic Fluid Volume 252
Polyhydramnios (Hydramnios) 252
Oligohydramnios 254

xv
TABLE
OFCONTENTS
CHAPTER
9:MEDICAL
ISSUES
INPREGNANCY
Section 1: Overview of the Medical Issues in Pregnancy 259
Section 2: Hypertensive Disorders in Pregnancy 261
Section 3: Hematologic and Immunologic Disorders 273
Physiologic Anemia in Pregnancy 273
Iron Deficiency Anemia in Pregnancy 274
Megaloblastic Anemia 276
Antiphospholipid Antibody Syndrome 276
Section 4: Endocrinologic Disorders in Pregnancy 280
Gestational Diabetes Mel\itus 280
Hyperthyroidism in Pregnancy 284
Hypothyroidism in Pregnancy 286
Section 5: Lung Disorders and Infection in Pregnacny 288
Bronchial Asthma in Pregnancy 288
Pneumonia in Pregnancy 289
Urinary Tract Infection (UT!) in Pregnancy 290
Sexually Transmitted Infections in Pregnancy 292
Non-sexually Transmitted Infections in Pregnancy 295

CHAPTER
10:APPROACH
TOPATIENTS
INGYNECOLOGY
Section 1; Gynecologic History and Examination 303
Approach to Patients in Gynecology 303
The Gynecologic History 305
The Gynecologic Examination 307
Section 2: Procedures in Gynecology 311
VuIvar Dermal Biopsy and Vaginal Smear 311
Pap (Papanicolaou) Smear 313
Colposcopy 318
Endometria\ Sampling 320
Other Common Procedures in Gynecology 322

CHAPTER
11:BENIGN
GYNECOLOGIC
DISEASES
Section 1: Benign Diseases of the Vulva and Vagina 327
Dermatologic Diseases 327
Benign Cysts & Tumors 329
Section 2: Benign Diseases of the Cervix, Uterus, and Fallopian Tubes 332
Diseases of the Cervix 332
Endometrial Polyp 333
Leiomyoma 333
Paratubal Cysts 336
Endometriosis 337
Adenomyosis 340
Section 3: Benign Disorders of the Ovaries 343
Functional Cysts of the Ovary 343
Benign Ovarian Tumors 344
General Approach to Adnexal Masses 345

CHAPTER
12:GENITAL
TRACT
INFECTIONS
Section 1: Overview of the Genital Tract Infections 349
Sexually Transmitted Diseases 349
Endogenous Infections 350
Iatrogenic Infections 350
Section 2: Lower Genital Tract Infections 351
Bartholin Gland Cyst and Abscess 351
VuIvar Infections 352
Genital Ulcers 353
Vaginitis 358
Cervicitis 360
Section 3: Pelvic Inflammatory Disease 362
Overview of Pelvic Inflammatory Disease 362
Management of PIO 363

CHAPTER
13:PELVIC
FLOOR
Section 1: Overview of Anatomy and Physiology of Pelvic Floor 367
Anatomy of the Pelvic Floor 367
Physiology of Voiding 368
Section 2: Pelvic Organ Prolapse 369
Pathogenesis and Manifestations of POP 369
Pelvic Organ Prolapse Quantification System 370
Management of POP 373
Section 3: Urinary Incontinence 375
Overview of Urinary Incontinence 375
Management of Urinary Incontinence 377
XVI
TABLE
OFCONTENTS
CHAPTER
14:CONGENITAL
ANOMALIES
OFTHEFEMALE
REPRODUCTIVE
TRACT
Section 1: Overview of the Congenital Anomalies 381
Section 2: Congenital Anomalies of the Uterus 384
AFS Class I: Agenesis 384
AFSClass II: Unicornuate Uterus 385
AFS Class lll: Uterine Didelphys 385
AFS Class IV: Bicornuate Uterus 386
AFS Class V: Septate Uterus 386
AFS Class VI: Arcuate Uterus 387
AFS Class Vil: Diethylstillbestrol Related Anomalies 387
Section 3: Congenital Anomalies of the Vagina and Vulva 388
Longitudinal Vaginal Septum 388
Transverse Vaginal Septum 389
Vaginal Atresia 389
lmperforate Hymen 390
Microperforate Hymen 390
Labial Hypertrophy 390

CHAPTER
15:PEDIATRIC
GYNECOLOGY
Section 1: Overview of Pediatric/Adolescent Gynecology 395
Reproductive Tract of Children & Adolescents 395
Puberty 396
Gynecologic Examination 397
Section 2: Disorders of Sexual Maturation 399
Advanced Sexual Maturation (Precocious Puberty) 399
Delayed Sexual Maturation 404
Section 3: Disorders of Sexual Development (DSD) 405
Errors in Sexual Determination 405
Section 4: Menstrual Disorders 408
Abnormal Uterine Bleeding (AUB) 408
Primary Dysmenorrhea 408
Section 5: Other Disorders in Pediatric Gynecology 409
Vulvovaginitis 409
Urethral Prolapse 409
Foreign Bodies 410
Labial Adhesions 410
Lichen Sclerosus 411
Vaginal Bleeding 411
Section 6: Gynecologic Tumors 412
Overview of Gynecologic Tumors 412
Tumors of the Vulva, Vagina, and Cervix 412
Tumors of the Ovaries 413

CHAPTER
16:REPRODUCTIVE
GYNECOLOGY
Section 1: Amenorrhea 417
Primary Amenorrhea 418
Secondary Amenorrhea 422
Section 2: Menstrual Abnormalities 425
Dysmenorrhea 425
Premenstrual Syndrome & Premenstrual Dysphoric Disorder 427
Section 3: Abnormal Uterine Bleeding 429
Review of the Normal Menstrual Pattern 429
Overview of Abnormal Uterine Bleeding 429
FlGO (PALM-COElNJ Classification System of AUB 430
Approach to Abnormal Uterine Bleeding 433
Section 4: Polycystic Ovary Syndrome 436
Section 5: Infertility 442
Evaluation and Diagnosis of Infertility 442
Approach to Female Factor Infertility 443
Approach to Male Factor Infertility 447
Intrauterine Insemination 448
Assisted Reproductive Techniques 448
Section 6: Menopause 451
Manifestations of Menopause 451
Management of Menopause 452
Section 7: Fertility Preservation 455
Gonadotoxicity of Cancer Therapy 455
Management Options 455

XVII
TABLE
OFCONTENTS
17:FAMILY
CHAPTER PLANNING
Section 1: Overview of Family Planning 463
Comparing Effectiveness of Family Planning Methods 464
Medical Eligibility 466
Section 2: Natural Family Planning Methods 467
Sexual Abstinence 467
Coitus lnterruptus 467
Fertility Awareness Methods 468
Section 3: Hormonal Contraception 470
Combined Hormonal Contraceptives 470
Progestin-Only Contraceptives 473
Section 4: Intrauterine Devices 475
Section 5: Barrier Methods 477
Section 6: Sterilization 478
Female Sterilization 478
Male Sterilization 480
Section 7: Emergency Contraception 481

CHAPTER
18:GYNECOLOGY
ONCOLOGY
Section 1: lntraepithelial Neoplasia of Lower Genital Tract 485
Etiopathogenesis 485
Prevention 487
Cervical Cytology Reporting (Bethesda System) 489
Cervical lntraepithelial Neoplasia (CIN) 493
Cervical Adenocarcinoma in Situ 494
Vulvar Atypia 495
Section 2: Cervical Carcinoma 497
Cervical Carcinoma 497
Manifestations and Staging 498
Management 500
Section 3: Neoplastic Lesions of the Uterus SOI
Endometrial Hyperplasia 501
Endometrial Cancer 504
Section 4: Ovarian Cancer 507
Etiopathogenesis 507
Manifestations and Diagnosis 509
Germ Cell Tumors 511
Sex Cord Tumors 512
Section 5: Vulvar Cancer 513
Etiopathogenesis 513
Diagnosis 513
Management 515

CHAPTER
19:GESTATIONAL
TROPHOBLASTIC
DISEASE
AND
NEOPLASIA
Section I: Overview of Gestational Trophoblastic Diseases 519
Section 2: Benign Gestational Trophoblastic Diseases 520
Complete Hydatidiform Mole 520
Partial Hydatidiform Mole 520
Section 3: Gestational Trophoblastic Neoplasia 524
Invasive Mole 524
Choriocarcinoma 524
Placental Site Trophoblastic Tumor 527
Epithelioid Trophoblastic Tumor 527

CHAPTER
20:SOARD
CORRELATES
Section I: Obstetrics 531
Section 2: Gynecology 543

XVIII
ANATOMY
AND
PHYSIOLOGY
OFTHE
FEMALE
REPRODUCTIVE
SYSTEM
 SECTION
ANATOMY OF THE FEMALE REPRODUCTIVE TRACT
ONE
I
ANATOMY OF THE FEMALE REPRODUCTIVE SYSTEM
• Organs of the female reproductive tract are divided into the external and internal
genitalia (see below)
• Reproductive organs are in intimate contact with the lower urinary tract & large intestines

Uterine cavity

Cervix
Fallopian
tube
Fimbriae
Ovary

Bladder
ll':ltr-:-+s------h~'llf--+----- Cervix

\\..,_.....,.,.,..."':;,fi1'f--.W-------f'+-------+ Vagina
'\..-4---,-tl½-I------+ Urethra
1/--:::~~~~~,------ Rectum

I. SUBDIVISIONS OF THE FEMALEREPRODUCTIVE ORGANS

EXTERNAL GENITALIA
(outside the true pelvis)
I INTERNAL GENITALIA
(within the true pelvis)
• Perineum • Vagina
• Mons pubis • Cervix
• Clitoris • Uterus
• Urethral (urinary) meatus • Uterine (fallopian) tubes
• Labia majora and minora • Ovaries
• Vestibule
• Greater vestibular (Bartholin) glands
• Skene glands
• Periurethral area

3
II. HOMOLOGOUS STRUCTURESBETWEENMALE& FEMALEREPRODUCTIVESYSTEMS
• Sex determination involves genetic, gonadal, and phenotypic sex:
0 Genetic sex (XXor XY): established at fertilization
0 Gonadal sex: heralded by differentiation of the primordial gonad into a testis or an ova1y
Phenotypic sex: differentiation of genitalia to the male phenotype is dependent on
testicular function (in the absence of a testis, female differentiation ensues)

I MALE
Genital ridge
Mesonephric ducts
Paramesonephric
ducts
Genital Tubercle
Urogenial sinus
Urogenital folds
Labioscrotal swelling
I FEMALE
• Testis • Ovary
• Epididymis, ductus deferens,
• Gartner duct
ejaculatory duct
• Prostatic utricle, appendix • Uterus, fallopian tubes, upper
of testis vagina
• Glans penis
• Glans clitoris
• Corpus cavernosum and
• Vestibular bulb
spongiosum
• Cowper glands
• Bartholin glands
(bulbourethral)
• Skene glands (paraurethral)
• Prostate gland
• Ventral shaft of penis • Labia minora
• Scrotum • Labia majora

VULVA (PUDENDA)
• Term used to describe the external organs visible in the perinea! area
• Includes all structures visible externally from the mons pubis to the perinea! body

Labia minora (paired) -----+------+_,,-r:.~IM---+-- Urethral meatus

~·1,,11r-1f-.+-- Vestibule
--,F-++----"~t. 'hwrr--.i~+~- Vagina I orifice

Structures of the Vulva:

• Mons pubis • Hymen
• Clitoris • Vaginal opening
• Urinary meatus • Urethral opening
• Labia majora and minora • Glandular structures
• Vestibule

I.MONS PUBIS
• Rounded fatty prominence anterior to the pubic symphysis, pubic tubercles, and superior
pubic rami
• Formed by a mass of fatty subcutaneous tissue covered with pubic hairs after puberty
• Surface is continuous with the anterior abdominal wall
4
II. LABIA MAJORA AND MINORA

Description
I LABIA MAJORA
• Two longitudinal folds of adipose
& fibrous tissue which extend
I LABIA MINORA
• Two small cutaneous folds
between the labia majora and the
I
from mons pubis to perinea) body introitus ( or vaginal vestibule)
Lining • Outer: KSSE
• NKSSE
epithelium • Inner: NKSSE
• Lie in close apposition
Nulliparous • Not visible behind the
• Inner surface resembles the
women non-separated labia majora
mucous membrane
Multiparous • Gape widely
• Project beyond the labia majora
women • Inner surface become skin-like
• With hair follicles • No hair follicles
Glands • With sweat glands • No sweat glands
• With sebaceous glands • With sebaceous glands
KSSE:keratinizing
stratifiedsquamousepithelium
NKSSE:non-keratinizing stratifiedsquamousepithelium

III. HYMEN
• Thin membrane (NKSSE) at the entrance of the vaginal orifice that is normally perforated
to allow egress of menstrual blood and secretions
During first coitus, laceration usually occurs at the 6 o'clock position
• Caruncle myrtiformes: remnants of hymen in adult female

IV. CLITORIS
• Erectile structure found beneath the anterior joining of the labia minora
• Very sensitive structure made up of glans, a corpus or body and two crura, which attach
to the periosteum of the ischiopubic rami

V. VESTIBULE
• Almond shaped area between the clitoris and the vaginal introitus (opening)
• Functionally mature female structure of the urogenital sinus of the embryo
• Extends from clitoris to posterior fourchette

A. Glandular Structures in the Vestibule

PERIURETHRAL GLANDS
I "Skene glands"
I "Bartholin glands"
Other name • Lesser vestibular glands
Type of gland • Tubuloalveolar
Location • Adjacent to the urethra
Pathology • Urethral diverticulum
• Secrete lubrication at the
Function
opening of the urethra
VULVOVAGINAL GLANDS
• Greater vestibular glands
• Compound alveolar/ compound acinar
• 5 and 7 o'clock of the vagina
• Bartholin cyst/ abscess
• Responsible for lubrication to the
vagina, with openings just outside
the hymen, bilaterally, at the
posterior aspect of the vagina

8. Six Openings in the Vestibule

0 Vaginal introitus

0 Urethral opening
0 Paired Skene glands opening
0 Paired Bartholin ducts opening

s
INTERNAL GENITALIA

Intramural
Isthmus
,-----,
segment
-----~
Ampulla[ Uterine
body
,,·.-z.--.-
Infundibulum[ Uterine
FimbriaeC isthmus

*Endocervical
Lateral fornix ---~ canal
External os ------#--'

I. VAGINA
• Thin-walled, distensible, fibromuscular tube, 7-10 cm long that extends from the
vestibule of the vulva to the cervix
• Lined by rugae, which are situated in folds throughout
• Rugae in reproductive aged women has an accordion-like distensibility

A. Borders of the Vagina

Vesicovaginal septum
Rectovaginal septum
Rectouterine pouch of
Douglas
Upper vaginal vaults
• Separates the vagina from the bladder and urethra
• Separates the lower portion of the vagina from the rectum
• Separates the upper portion of the vagina from the rectum
• Subdivided into anterior, posterior, and two lateral fornices
by the uterine cervix
• Posterior fornix provides surgical access to the peritoneal cavity

B. Supply and Support

I UPPER 1/3
I MIDDLE 1/3 I LOWER 1/3
• Uterine or inferior
• Ce,·vical branch of the vesical arteries • Internal
Blood
uterine artery • Internal iliac artery pudenda)
supply
• Vaginal artery • Middle rectal artery artery
(posterior vaginal wall)
• Internal, external,
Lymphatics • Internal iliac nodes • Inguinal nodes
common iliac nodes
• General
• Sympathetic via hypogastric plexus
Nerves somatic via the
• Parasympathetics via S2-S4 (low density)
pudenda) nerve
• Levator ani muscle and
transverse cervical,
Support • Urogenital diaphragm • Perinea! body
pubocervical and
sacrocervical ligaments
6
II. CERVIX
• It is the !owe, and narrow portion of the uterus
• May vary in shape from cylindric to conical
• Usually 2.5-3 cm in length and 7-8 mm at its widest point
• Cervical canal opens into the vagina at the external os of the cervix
I
• Cervical canal opens into the uterine cavity at the internal os of the cervix

A. Histology
° Consists of predominantly fibrous tissue (in contrast to the primarily muscular corpus
of the uterus)
0 The transformation zone encompasses the transition from stratified squamous
epithelium to columnar epithelium (most cervical dysplasia develops within this
transformation zone)

B. Parts of the Cervix

0The vagina is attached obliquely around the middle of the cervix, dividing the cervix into:
• Upper portion: supravaginal portion
• Lower segment: portio vaginalis

I ENDOCERVlX I ECTOCERVIX
Location • Supravaginal portion • Portie vaginalis
• Extends from the isthmus
• Extends from the squamo-
(internal OS) to the ectocervix
Extent columnar junction to the
and contains the endocervical
external orifice
canal
• Single layer of mucus-secreting
highly ciliated columnar • Non-keratinized stratified
Histology epithelium which is thrown into squamous epithelium
folds forming complex glands • Hormone-sensitive
and crypts
Nervous supply • Extensive amount of nerves • Few nerves only
Blood supply • Cervicovaginal branch of uterine artery located at the lateral walls

II. UTERUS
• Thick-walled, hollow, muscular organ located centrally in the female pelvis
• Nullipara: ~8 cm long, 5 cm wide, and 2.5 cm thick and weighs 40-50 g
• Multipara: each measurement is approximately 1.2 cm larger and uterine weight is 20-30 g
heavier
• The maximal weight of a normal uterus is 110 g

A. Blood Supply, Lymphatic Drainage and Nerve Supply

• Uterine artery from internal iliac
0 Travels medially across pelvic floor then crosses the ureter
Arterial supply superiorly
0 To reach the uterus, it will pass above the vagina's lateral fornix
• Ovarian artery
Venous drainage • Uterine vein (going to internal iliac vein) and ovarian vein
Lymphatic • Paraaortic nodes: fundus
drainage • Internal and external iliac nodes: body and cervix
Innervation • Inferior hypo gastric plexus

7
 B. Histolol!V
Stratum Functionale
• Responds to fluctuating hormonal levels • Zona spongiosa
• Shed during menstruation
• Supplied by the spiral arteries
Endometrium • Zona compacta
• Superficial 2/3
Stratum Basale
• Supplied by the straight arteries
• Basal 1/3
• Inner longitudinal
Myometrium • Middle oblique
• Outer longitudinal ("hood-like" pattern)
Serosa • Visceral peritoneum

C. Sections of the Uterus

• Area between the corpus uteri & the cervix (cervico-corporeal junction)
• Short area of constriction in the lower uterine segment
Isthmus • lsthmus/cervicocorpal junction: during pregnancy, this is the area
that enlarges (28 weeks onwards] and becomes very dynamic (i.e.,
undergoes thinning, stretching)
• Rounded/dome-shaped portion on the top of the uterus (above a
Fundus
plane connecting the two fallopian tubes)
• Active segment: upper 2/3 of uterus where muscles are thick and
participates in contraction of uterus
Corpus Uteri • Passive segment: lower 1/3 of the uterus where myometrium is
thinner & does not participate in contraction (the former isthmus
becomes the lower uterine segment)

III. FALLOPIANTUBES
• The paired uterine tubes extend outward from the superolateral portion of the uterus and
open outwardly in close approximation to the ovaries
• They are between 10 & 14 cm in length and slightly <l cm in external diameter
• Each tube is divided into four anatomic sections
SEGMENT I DESCRIPTION I CLINICAL CORRELATES
• 2% of ectopic pregnancy
Intramural • 1 to 2 cm in length and is
• Ectopic pregnancy at this area
Interstitial surrounded by myometrium
result in severe maternal morbidity
• Most highly developed musculature
• Narrowest portion
• The narrow portion of the
• Preferred portion for applying
tube that adjoins the uterus,
Isthmus ligatures and clips for female
passes gradually into the
sterilization
wider, lateral portion
• Preferred portion for tubal ligation
I • 12% of ectopic pregnancy
• 4-6 cm in length & ~6 mm
in inside diameter; wider & • Site of fertilization
Ampulla
more tortuous in its course • 80% of ectopic pregnancy
than other segments
• Fimbriated extremity
Infundibulum • Tunnel shaped opening of the • 5% of ectopic pregnancy
distal end of the fallopian tube

8
 .
IV. OVARIES
• Lie on the posterior aspect of the broad ligament, in the ovarian Fossa
• Immediately adjacent to the ovarian fossa are the external iliac vessels, the ureter, and the
obturator vessels and nerves
• Attached to the broad ligament by the mesovarium
• Not covered by peritoneum
I
Mesovarium

Fimbria
Ovarian ligament
Mesometrium -------"~~.rr=~

A. Ligaments of the Ovary

LIGAMENT I DESCRIPTION
• Formed by the posterior portion of the broad ligament
• Attaches to the anterior border of the ovary
Mesovarium • Contains the arterial anastomotic branches of the ovarian &
uterine arteries, a plexus of veins, and the lateral end of the

-·
Ovarian ligament
lnfundibulopelvic
ligament (suspensory
ligament of the ovary)
ovarian ligament
• Narrow, short, fibrous band that extends from the lower pole
of the ovary to the uterus
• Forms the superior and lateral aspect of the broad ligament
• Contains the ovarian artery, veins, & accompanying nerves
• Attaches the upper pole of the ovary to the lateral pelvic wall

B. Supply and Drainage of the Ovaries

Ovarian arteries
Ovarian veins
Lymphatic drainage
• Arise directly from the aorta
• Accompany the arteries
• Left ovarian vein drains into the left renal vein
• Right ovarian vein drains into the inferior vena cava
• Aortic nodes

9
URETERS
• Muscular tubes, 28-34 cm in length, extending from renal pelvis to the urinary bladder
• Retroperitoneal in location
• Found on the medial leaf of the parietal peritoneum and in close proximity to the ovarian,
uterine, obturator, and superior vesical arteries

Clinical Correlates
• Since the ureter lies underneath the uterine artery, surgical compromise of the ureter may
occur during:
• Clamping or ligating of the infundibulopelvic vessels
• Clamping or ligating of the cardinal ligaments, or
• Wide suturing in the endopelvic fascia during an anterior repair
• Two of the classic ways to differentiate a ureter from a pelvic vessel are:
• Visualization of peristalsis after stimulation by a surgical instrument
• Visualization of Auerbach plexuses, which are numerous, wavy, small vessels that
anastomose over the surface of the ureter

GENERAL BLOOD SUPPLY OF THE FEMALE REPRODUCTIVE SYSTEM

I. ARTERIALBLOODSUPPLYTO THE FEMALEREPRODUCTIVESYSTEM
A. Major Blood Supply to the Organs of the Reproductive System
PART
I BLOOD SUPPLY
Pudenda • Internal pudenda! artery
• Upper 1/3: vaginal artery of the uterine artery
• Middle 1/3: uterine or inferior vesical arteries, internal iliac artery,
Vagina
and middle rectal artery (posterior vaginal wall)
• Lower 1/3: internal pudenda! artery
Cervix • Cervicovaginal branch of uterine artery
Uterus
Fallopian • Uterine artery
tubes • Ovarian artery
Ovaries

B. Participants in the Collateral Circulation of the Female Pelvis

SOURCE I BRANCHES
• Ovarian artery
• Inferior mesenteric
Aorta
• Lumbar and vertebral
• Middle sacral arteries
External iliac • Deep iliac circumflex
artery • Inferior epigastric artery
Femoral • Medial femoral circumflex artery
artery • Lateral femoral circumflex artery

II. VENOUSDRAINAGE OFTHEFEMALE REPRODUCTIVE SYSTEM

• Pelvis is drained mainly by the internal iliac vein and their tributaries
• Some occur through the superior rectal, median sacral, ovarian veins

10
_T_H_E_F_E_M_A_L_E_P_E_L_V_IS
_________________ , __
:
I. THE PELVICBONES
• The bony pelvis consists of the two hip bones, the sacrum and the coccyx
• The hip bone is an irregularly shaped bone, also known as the pelvic girdle
• Pelvis is divided into false and true compartments
° False pelvis: lies above the linea terminalis
0 True pelvis: lies below the boundary

A. There are Four Articulations within the Pelvis:

Two sacroiliac joints: between the ilium of the hip bones, and the sacrum
0

Sacrococcygeal symphysis: between the sacrum and the coccyx

0

• Pubic symphysis: between the pubic bodies of the two hip bones

CONJUGATES

True conjugate A

Obstetricalconjugate B
Diagonalconjugate
Sacral

Sacral promontory

LIGAMENTS

Sacrospinous
Pubic symphysis spines ligament

Transverse of inlet A 13.S cm Sacrotuberous

lnterspinous diameter B 10 cm ligament

Obstetrical conjugate C 10.S cm

Obturator Lesser Greater

FORAMENS
foramen sciatic foramen sciatic foramen

Four Bones of the Pelvis

• Two innominate bones (fusion ofischium, ilium, and pubic bones]
• Sacrum
• Coccyx

Four Imaginary Planes of the Pelvis:

• Plane of the pelvic inlet (superior strait)
• Plane of the pelvic outlet (inferior strait)
• Plane of the midpelvis (least pelvic dimensions]
• Plane of greatest pelvic dimension (of no obstetrical significance)

B. Anteroposterior Conjugates of the Pelvic Inlet

True • Measured from sacral promontory to the upper part of the pubic symphysis
Conjugate • Normally 11 cm
Diagonal
• Measured from sacral promontory to lower part of pubic symphysis
Conjugate
• Only conjugate that can be measured clinically
(DC)
Obstetric • Measured from Sacral Promontory to mid-portion of Pubic Symphysis
Conjugate • Computed using the diagonal conjugate minus 1.5 to 2 cm (OC= DC- 1.5 to 2)
(OC) • Important in parturition
11
II. CALDWELL-MO
LOYCLASSIFICATION
• A line passing through the widest transverse diameter divides the inlets into posterior (P)
and anterior (A) segments

--."J·~./-,.
i ,.; "-.J;-
-- \
'O~<T'

8 ·e5 "ej" EB
Pelvic Inlet
Antero- Transversely
Shape Round Triangular
posteriorly; oval oval
AP-Segment Equal & spacious Posterior< anterior Posterior< anterior Flat
>90° inclined >90° inclined <90° inclined >90° inclined
Sacral Angle
backwards backwards forward backwards
Sacrum Curved Curved Straight Straight
Pelvic Ca_vity
Sacrosciatic notch Wide & shallow Wider, shallower Narrow & deep Narrow & small
Straight or Straight or
Side Walls Convergent Divergent
divergent divergent
Pelvic Outlet
Lachial Spines Not prominent Not prominent Prominent Not prominent
Pubic Arch Curved Long & curved Long & straight Short & curved
Subpubic Angle Wide Slightly narrow Narrow Very wide
Bituberous
Normal Normal/short Short Wide
Diameter

III. OBSTETRICOUTCOMESOF EACHPELVISTYPE

Occipito-lateral Direct occipito- Occipito-lateral

Position or oblique anterior or or Oblique Occipito-lateral
occipitoanterior posterior Occipitoposterior
Diameter of Transverseor Transverseor
Antero-posterior Transverse
Engagement oblique oblique
No difficulty;
Delayed &
Engagement No difficulty except flexion is Difficult
difficult
delayed
Pelvic Cavity
Internal Difficult anterior
Anterior rotation
Rotation rotation
Pelvic Outlet

Difficult delivery
Face-to-pubis with increased
Delivery No difficulty No difficulty
delivery chance of perinea!
injuries

12
_D_IA_P_H_RA_G'-'M'---A-'-N_D_L_IG--'-'--'A-"-M=E"-'N~T..;;;.S
______________ I_=.
I.DIAPHRAGM
COMPONENT I REMARKS
• Wide but thin muscular layer of tissue that forms the inferior border
of the abdominopelvic cavity
• Composed of a broad, funnel-shaped sling of fascia & muscle
• Extends from symphysis pubis to the coccyx & from one lateral
sidewall to the other
Pelvic
• Major muscles:
diaphragm
° Coccygeus
(endopelvic
0Levator ani (pubococcygeus, puborectalis, and iliococcygeus)
fascia)
• The paired levator ani muscles act as a single muscle and functionally
are important in the control of urination, in parturition, and in
maintaining fecal continence
• Supports abdominal & pelvic viscera & facilitates equal distribution of
intraabdominal pressure (e.g., during coughing, straining)
Urogenital
• Strong, muscular membrane that occupies the area between the
diaphragm
symphysis pubis and ischial tuberosities
(triangular
• Support the urethra and maintain the urethrovesical junction
ligament)

II. LIGAMENTS
• Ligaments attach the lateral border of the sacrum to various bony landmarks on the bony
pelv;s to aid stability
• Two wing-like membranous ligaments that extend from the lateral
margins of the uterus to the pelvic walls
Transverse cervical/cardinal: pass to the cervix and upper part of
0

the vagina
Broad ligament Pubocervical: from posterior surface of the pubis to the cervix;
0

position on both sides of the neck of the bladder

Sacrocervical: from lower end of sacrum to the cervix and upper
0

end of vagina
• Divide the pelvic cavity into anterior and posterior compartments
• Provide the major support of the uterus and cervix
Cardinal • Originated from the densest portion of the broad ligament
ligament • Medially united to the supravaginal wall of the cervix
• Maintains anatomic position of the cervix & upper part of the vagina
• From posterolateral to the supravaginal portion of the cervix
Uterosacral
encircling the rectum then inserts into the fascia over S2 and S3
ligament
• Provides anatomic support to the cervix
• Extend from the lateral portion of the uterus, arising below and
anterior to origin of the oviducts, that is continuous with the broad
Round Ligament
ligament, outward and downward to the inguinal canal terminating at
upper portion of labia majora

13
CLINICAL CORRELATES
CLINICAL SCENARIO
Radical hysterectomy
Iliac and obturator node
dissection
Improper placement of legs in
the stirrups or prolonged dorsal
lithotomy position
Damage due to pressure from
lateral blade of a self-retaining
retractor during an abdominal
hysterectomy/ inguinal node
dissection
Node dissection of the obturator
fossa
Straddle or after giving
anesthetic for second stage labor
I ANATOMICAL
INVOLVEMENT I REMARKS
• Anesthesia/hypoesthesia
• Genitofemoral nerve
or pain at the perineum
• Interfere with adduction of
the thigh and hip
• Obturator nerve
• Sensory function on the
medial aspect of the thigh
• Footdrop
• Peroneal nerve • Sensory and motor loss
over the lateral lower leg
• Prohibits flexion of the hip,
• Femoral nerve patient is not able to lift leg
off the bed
• Severe blood loss if
• External iliac artery
transected
• Injury producing a very
• Pudenda! artery
large hematoma
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition.2018
14
 SECTION
THE MENSTRUAL CYCLE
REVIEW OF THE HYPOTHALAMIC-PITUITARY-OVARIAN
TWO

(HPO) AXIS
I
• The HPO axis is a tightly regulated system controlling female reproduction & physiology
• The axis coordinates a tightly regulated feedback loop that consists of:
0Gonadotropin-releasing hormone (GnRH) produced by the hypothalamus
Follicle-stimulating hormone (FSH) & luteinizing hormone (LH) from anterior pituitary
Sex steroids (e.g., estrogen, progesterone) from the ovaries

Positive
I feedback
I Follicular
···························►Q ANTERIOR
+--
I phase
:························•''. ~ PITUITARY I

LH
FSH
Negative
feedback
i.0·· Activin
OVARIES Luteal
···O··lnhibin phase

I
Estradiol
Progesterone
-0-1
• The hypothalamus secretes GnRH
• In response to GnRH stimulation, the anterior pituitary produces LH and FSH
• FSH and LH act primarily to activate the ovaries to produce estrogen, progesterone, &
inhibin and to regulate the menstrual and ovarian cycle.

L GONADOTROPIN-RELEASING HORMONE(GnRH)
Regulates secretion of FSH and LH
• Secreted in pulsatile manner to be effective
• Released from neurons within the anterior hypothalamus (arcuate nucleus of the median
basal hypothalamus)

II. GONADOTROPINS:FSH AND LH

• Structural similarity- identical a subunits, different p subunits
• FSH: acts on the granulosa cells of the ovarian follicles to stimulate follicular growth
• LH: acts on the theca cells and on the granulosa cells, which are luteinized to theca-lutein
and granulosa-lutein cells respectively, to stimulate ovarian steroid production

15
III. OVARIAN
STEROIDS
• Biosynthesis of the ovarian steroids
• Following binding of the gonadotropins to their receptors, steroid production begins in
the ovary
• Three principal sex steroids of the ovary:
Estradiol
Progesterone
0Androgen
HORMONE I ACTIONS
• Represents a group of hormones including:
• Estrone: most common form in the post-menopausal years
• Estradiol: most potent; most common form during reproductive years
Estrogen • Estriol: least potent; most common form in pregnancy
• Secretion is regulated by FSH
• For development of secondary sex characteristics at puberty
• Thickens endometrium during the proliferative phase
• Secretion is regulated by LH
Progesterone • Maintains endometrium during secretory phase
• Prepares endometrium for implantation (during pregnancy)
• Androstenedione & testosterone are produced in the theca cells
• Regulated by LH
• At low concentrations, these are transported to the granulosa cells
for aromatization to estradiol & estrone (two-cell two-gonadotropin
Androgen
mechanism of steroidogenesis)
• At high concentrations (such as in PCOS), they are converted to 5-alpha
reduced androgens that cannot be converted to estrogens and inhibit
aromatase activity (this causes the atresia of follicles)

OVERVIEW OF THE MENSTRUAL CYCLE

• More accurately called "female monthly sexual cycle"
• Spontaneous, cyclical ovulation occurs at 21- to 35-day intervals
• Cyclical ovulation continues for almost 40 years between menarche and menopause
• There are ~400 opportunities for pregnancy, which may occur with intercourse on any of
1,200 days (includes day of ovulation and its two preceding days)
• Menstrual cycle days 20 to 24 is the narrow window of endometrial receptivity to
blastocyst implantation

Components of the Menstrual Cycle

• The menstrual cycle involves cyclic changes in two organs:
0Ovary (ovarian cycle)
0Uterus (endometrial cycle)
It may be divided in 14-day phases:

Endometrial Cycle • Proliferative • Secretory • Changesin endometrium

'Assumesa 28 daycycle

Normal Dimensions of Menstruation

PARAMETER
I NORMAL VALUE
Frequency of menses • Every 24 to 38 days
Duration of menses • 58 days
Regularity of menses • Shortest to longest cycle variation is ,; 7-9 days
Flow volume • <80 mL blood loss per cycle
Source:MunroMG,CntchleyHO,Fraser,IS Int J GynecolObstet2018
16
~O_v_e_r_v_ie_w_oa.,J_t_h_e_M_e_n_s_t_r_u_a_l_Ca.y_c_Ie
_______________________ -, I
,..,.
ro
3
-0 OJ
ro o
~ 0..
~<
C
nl

:::,-
0 0
3 ~
g ~-
ro ::::,
V>

0
n
<n
<
OJ
~
ro w·
::::,

m
::::,
0..
~ 0
n 3
ro ~
iii"

Menses Proliferative; Secretory I Menses

DO D14 D28
FOLLICULAR PHASE LUTEAL PHASE

• Ovarian-endometrial cycle has been structured as a 28 day cycle

• The follicular phase (days 1-14) is characterized by increasing estrogen, endometrial
thickening, and selection of the dominant ovulatory follicle
• In the luteal phase (days 14-28), the corpus luteum produces estrogen & progesterone,
which prepare the endometrium for implantation
• If implantation occurs, the developing blastocyst begins to produce human chorionic
gonadotropin (hCG), prolonging the lifespan of the corpus luteum, which produces
progesterone until the placenta takes over
• In the absence of pregnancy, the corpus luteum rapidly regresses 9-11 days after ovulation
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition.2018

17
OVARIAN CYCLE

I ESTROGEN I PROGESTERONE
I FSH I LH
Menstruation L L L L
Follicular phase i L i L
Ovulation i L i i
Luteal phase L i L L
Key Points to Remember:
• Dropin progesteronelevelstriggermenstruation
• Estrogenis the mainhormoneduringthe follicular
phase;itcauses selectivenegativefeedback
• Progesteroneis the mainhormoneduringthe lutealphase;itcauses non-selective negativefeedback
• EstradiolsurgeprecedesLHsurge
• LHsurgeis the triggerforovulation;
alsotriggersluteinization
of granulosacellsintoLHreceptivecells(enabling
granulosacellsto respondto LH levelsand produceprogesterone)
• FSHas the nameimpliestriggersfolliculardevelopment

I. FOLLICULAR PHASE
• First phase which involves the maturation of follicles
• Begins with the initiation of menstruation and averages 14 days in length
• The length of the follicular phase determines the cycle duration
• Can be divided into three distinct phases:
PHASE I REMARKS
Recruitment • The withdrawal of estrogen & progesterone during the luteal phase
of cohort of of the prior cycle causes a gradual increase in FSH,which stimulates
antral follicles growth of primordial ovarian follicles
• Of the primordial follicles, one becomes the dominant follicle &
develops/matures until ovulation
• It is usually the follicle that has the most vascularized theca layer and a
Selection of
higher number of gonadotropin receptors
a dominant
follicle • Follicular phase estradiol production is explained by the two-cell
two-gonadotropin mechanism (see below)
• Elevated estradiol activate the negative feedback loop, resulting to
decreased FSH that cannot sustain the growth of other follicles
Growth of • The developing dominant follicle, destined to ovulate, produces
the dominant estrogen that enhances follicular maturation & increases production of
follicle gonadotropin receptors

( ) ORCUIATION I

• Two Cell-Two Gonadotropin Theory states that there is compartmentalization of steroid

hormone synthesis
• The theca cells, under the stimulation of LH,produces androsteinedione & testosterone which
are transported to granulosa cells for FSHstimulated aromatization into estrone & estradiol
18
II. OVULATION
• Toward the end of the follicular phase, estrogen levels eventually surge to reach a critical
level that triggers the anterior pituitary to release an LH spike.
• A sustained high level of estrogen >200 pg/ml for >48 hours is required to produce a
positive feedback on LH release
• The LH surge triggers the resumption of meiosis in the oocyte and induces production of
I
progesterone and prostaglandins within the follicle
• The progesterone and prostaglandins, in turn, are responsible for the rupture of the
follicular wall with release of the mature ovum or ovulation
• After releasing the ovum, corpus luteum is formed

III. LUTEALPHASE
• This phase coincides with the secretory phase of the endometrial cycle
• Granulosa cells and theca cells hypertrophy and the follicle wall collapses; the structure
becomes the corpus luteum
• The corpus luteum secretes: progesterone, estradiol, and inhibin A
• The lifespan of the corpus luteum is 9-11 days; it may be prolonged by hCG in early
pregnancy, which serves to maintain the vital steroidogenic function of the corpus luteum
until the time that the placenta takes over
• The luteal phase is relatively constant at 14 days post-ovulation, regardless of cycle
duration

IV.LUTEAL- FOLLICULAR TRANSITION

• If pregnancy does not occur, the demise of the corpus luteum causes a decrease in the
levels of inhibin-A, estradiol, & progesterone; this in turn removes the negative feedback
inhibition on the pituitary
• There is an increase in the GnRH pulse frequency and FSH secretion that causes a new
cohort of follicles to be recruited

19
ENDOMETRIAL CYCLE
• Includes proliferative, secretory, and menstrual phase
• Ovarian hormones drive morphologic and functional changes of endometrium

I. PROLIFERATIVE PHASE
• Coincides with the follicular phase
• There is progressive mitotic growth of the decidua functionalis as a result of the rising
estradiol level (secondary to the growth of the dominant follicle)
• Endometrial glands become longer and tortuous
• Before ovulation, subnuclear vacuoles appear at the base of the glands

II. SECRETORYPHASE
• Coincides with the luteal phase of the ovarian cycle (where corpus luteum comes into play)
• The endometrium is optimally prepared for implantation by day 6-7 post ovulation
0 In a regular 28-day cycle, the endometrium has well-formed subnuclear glycogen-rich
vacuoles in gland lining cells and palisading cell nuclei by day 17
0 The glands become increasingly elongated, tortuous and sacculated and the spiral
arterioles are in abundance
0 There is also stromal edema

III. MENSTRUATIONPHASE
• lfno implantation takes place and there is no hCG to maintain the corpus luteum, the
withdrawal of estrogen and progesterone causes the subsequent ischemia and autolysis
of the stratum functionalis that results in menstruation
• PGF2 alpha:
Theorized to facilitate the expulsion of the sloughed endometrial tissue from uterus
° Causes arteriolar spasm, endometrial ischemia, and myometrial contractions

20
 SECTION
MATERNAL ADAPTATIONS TO PREGNANCY
THREE
I
OVERVIEW
• Pregnancy is a period of adjustment to the demands and products of conception
• Profound local and systemic changes in maternal physiology are initiated by conception
and continue throughout pregnancy
• After delivery and expulsion of the placenta, these changes are rapidly reversed
Changes in pregnancy occur for the following reasons:
Maintain the pregnancy
Protect the fetus from toxic and harmful agents
Maintain the health of the fetus and mother
Protect the mother from deleterious effects of the maternal changes itself and eventual
delivery

CHANGES IN THE REPRODUCTIVE TRACT

I. UTERUS
• With pregnancy progression, the uterus leaves the pelvis & ascends to abdominal cavity
• Uterus progressively becomes soft as early as 6 weeks
• Hegar sign: softening of the isthmus
• Dextro-rotation: uterus rotates slightly to the right due to the rectosigmoid on the left
• Endometrium becomes specialized & is called the decidua (i.e., endometrium of pregnancy)

A. Changes in the Shape and Size of the Uterus

With pregnancy, uterus becomes a thin-walled muscular organ of sufficient capacity to
0

accommodate the fetus, placenta, and amniotic fluid

At 12 weeks, the gravid uterus becomes palpable above the pubic symphysis and
0

becomes an abdominal organ

At 20 weeks, the gravid uterus is at the level of the umbilicus
0

At 20-34 weeks, the fundic height in centimeters correlates with the AOGin weeks
0

Enlargement is due to the stretching and marked hypertrophy of muscle cells

0

• During first trimester: hypertrophy is stimulated by estrogen and progesterone

• After first trimester: uterine growth is mostly exerted by the expanding products of
conception

B. Uterine Contractility
Braxton-Hicks contractions: infrequent, unpredictable, sporadic, non-rhythmic
0

contractions, which increase progressively as the pregnancy approaches term

C. Uteroplacental Blood Flow

0 Nitric Oxide (NO):potent vasodilator which has a central role in reduced vascular resistance
0 Normal pregnancy has vascular refractoriness to the pressor effects of angiotensin II,
leading to increased uteroplacental blood flow
0 Hormones and growth factors that augment NO synthesis and production:
• Estrogen
• Progesterone
•Activin
• Placental Growth Factor (PIGF)
• Vascular Endothelial Growth Factor (VEGF)

21
II. CERVIXAND VAGINA
• Estrogen and progesterone makes the cervix swollen and softer during pregnancy
• Towards labot; the cervix decreases in length and opens (in preparation for birth)
• Estradiol stimulates growth of columnar epithelium of cervical canal, leading to ectropion (i.e.,
extension of endocervical glands onto ectoce1vical pmtion), making it prone to contact bleeding
• Chadwick sign: greater vascularity & hyperemia in the skin and muscles of perineum,
vulva, vagina, and cervix resulting in a characteristic violet color ("violaceous" appearance)
• Goodell sign: softening of the cervix (at 6-8 weeks AOG)
• Hegar sign: softening of isthmus

~ ~
~- -=-.

'""'""~1'1
_ ......
Externalas-- -- - - ------------ --
~

· - ---- - - - - - -- --- - - -·

III. OVARIES
• Ovulation ceases during pregnancy and maturation of new follicles is suspended
• Ovarian hormones play a crucial role during pregnancy
• Corpus luteum persists up to 8 weeks (which produces progesterone) and is completely
obliterated by 20 weeks AOG (luteo-placental shift)

CHANGES IN THE BREAST AND SKIN

I. BREAST
• Early pregnancy: breast tenderness and paresthesias
• After 2nd month: increase in size and delicate veins are visible just beneath the skin;
nipples become larget; more deeply pigmented, and more erectile
• End of pregnancy and early puerperium: colostrum is produced (thick, yellowish fluid
which can often be expressed by gentle massage)
• Glands of Montgomery: hypertrophic sebaceous glands scattered through each areola

II. SKIN
• Hyperpigmentation in pregnancy: maybe due to estrogen and progesterone increasing
melanocyte-stimulating hormone (MSH) during pregnancy
CHANGES IN
PREGNANCY
I DESCRIPTION

Striae gravidarum or • Reddish, slightly depressed streaks seen in the abdominal skin and
stretch marks over the skin of breasts and thighs
• Rectus muscles separate in the midline
Diastasis recti • Due to muscles of the abdominal wall not able to withstand the
tension of the expanding pregnancy
Linea nigra • Pigmented skin line in the midline of the anterior abdominal wall
Chloasmaormelasma
gravidarum ("mask • Irregular brownish patches of varying size on the face and neck
of pregnancy")
• Commonly seen on the face, neck, upper chest, and arms
Angiomas or
• Minute, red skin papules with radicles branching out from a central lesion
vascular spiders
• Likely from increased estrogen
• Redness in of the thenar and hypothenar eminences of the palms
Palmar erythema
• Due to increased estrogen
Telogen effluvium • Excessive hair loss in the puerperium
22
_M_E_TA_B_O_L_I_C_C_H_A_N_G_E_S_D_U_R_l"'-N-'-G--'-P_R_E_G_N_A_N_C_Y
_________ __ =.

• In response to the demands of the rapidly growing fetus and placenta, the pregnant
woman undergoes numerous metabolic changes

I. WEIGHTGAIN
• Metabolic alterations occur in pregnancy as a result of increased demands of the growing
fetus & placenta
• Average weight gain during pregnancy is 12.5 kilograms or 27.5 pounds

II. WATERMETABOLISM
• There is greater water retention in pregnancy
• Mediated by decreased plasma osmolality of 10 mOsm/kg, relaxin and other hormones
• At term:
Volume of fetus, placenta, and amniotic fluid is ~3.5 L
Expanded maternal blood volume from uterus and breast growth (~3.0 L)
, Pitting edema of the ankles and legs due to greater venous pressure from partial vena
cava occlusion by the enlarging uterus

III. PROTEINMETABOLISM
• The placenta regulates the amino acid concentrations - it is higher in the fetal than in the
maternal compartment
• Daily requirements for dietary protein intake during pregnancy are increased.

IV.CARBOHYDRATE METABOLISM
• Normal pregnancy characterized by:
0 Mild fasting hypoglycemia
0 Postprandial hyperglycemia
0 Hyperinsulinemia
• This is secondary to pregnancy-induced peripheral insulin resistance
, This is needed to ensure sustained postprandial glucose supply to the fetus
, Factors involved: progesterone, placentally derived growth hormone, prolactin,
cortisol, tumor necrosis factor, leptin

V. FATMETABOLISM
• Increased concentrations of lipids, lipoproteins, and apolipoproteins in plasma
, Secondary to increased insulin resistance
, Positively correlated with levels of estradiol, progesterone, and hPL
• Functions ofhyperlipidemia in pregnancy:
0 Aids in fat metabolism by the fetus
, Preparatory factor in milk production
• Fat storage in pregnancy:
Functions to protect the mother and the fetus during times of prolonged starvation of
hard physical exertion
, Primarily during mid-pregnancy; in central rather than peripheral tissues

23
VI. ELECTROLYTES
AND MINERALS

I REMARKS I INCREASEDI DECREASED

• Fetus imposes a significant demand on
Total serum Ca'• maternal calcium homeostasis; dietary
levels intake of calcium has to be increased to ✓
prevent excess depletion
• Although the GFRis increased, the
Serum Mg'• levels
excretion of Mg'•, Na•, and K' are ✓
unchanged due to enhanced tubular
Serum Na•levels
resorption ✓
• The concentrations are decreased slightly
Serum K"levels because of expanded plasma volume ✓
• Iron requirement is increased to meet the
Iron
requirement
expansion of maternal hemoglobin mass & ✓
the needs of fetal growth
• Iodine requirements increases because:
0 Maternal thyroxine production increases
to maintain euthyroidism and transfer
Iodine
requirement
thyroid hormones to the fetus ✓
0 Increase in fetal thyroid hormone
0 Increase in iodide glomerular filtration
rate

CHANGES IN THE HEMATOLOGIC SYSTEM

I. CHANGESIN THE BLOODVOLUME
• 40-45% increase in blood volume from non-pregnant state at 32-34 weeks AOG
• Pregnancy-induced hypervolemia serves several functions:
Meets metabolic demands of enlarged uterus, placenta and fetus
Provides abundant nutrients and elements to support the rapidly growing placenta and fetus
Protects the mother and fetus against the deleterious effects of impaired venous return
in the supine and erect positions
0 Buffers against adverse effects of parturition-associated blood loss

II. BLOODCELLS
A. Red Blood Cells (RBC)
RBC mass begins to increase at 8-10 weeks AOGand steadily rises
0

The increase in RBC mass is smaller than the increase in plasma volume, which
0

contributes to the physiologic anemia of pregnancy

During pregnancy, total iron requirement increases to 1000 mg (iron stores of healthy
0

non-pregnant woman is 300 mg)

B. White Blood Cells (WBC)

Pregnancy is associated with leukocytosis (or increase in WBC count) and approaches
0

15,000 to .;,25,000/uL during labor and early puerperium

C. Platelets
0 Platelet counts decline as pregnancy progresses, but usually remain in the normal range
0 Thrombocytopenia during pregnancy is partly due to hemodilution

III. COAGULATION & FIBRINOLYSIS

• Pregnancy is a procoagulant (prothrombotic) state
• Most evidence suggest decreased fibrinolytic activity that favors fibrin formation
• This ensures hemostatic control especially during delivery when blood loss is expected
INCREASES DURING PREGNANCY I DECREASES DURING PREGNANCY
• Fibrinogen • tPA (plasminogen activator)
• Factor VII • Anti-thrombin Ill (anticoagulation)
• Factor X • Protein C (anticoagulation)
• Plasminogen • Total protein S (anticoagulation)
24
_C_H_A_N_G_E_S_I_N_T_H_E_C_A_R_D_I_O_V_A_S_C_U_L_A_R_S_Y_S_T_E_M
_________ __ •.
I. HEMODYNAMICS
A. Overview of Hemodynamic Changes

--;:;160
;:,,
~
...140
C
Cardiac
output
"'
C
bO
~ 120
Q.
C.
0 Mean BP
C 100
0 ...
.,
C
80
SVR
<l.
.,
~

60
0 8 16 24 32 40
Weeks of pregnancy

The Major Hemodynamic Changes in pregnancy include:

0 Increased cardiac output by 30-50%
0 Expanded blood volume
0 Reduced systemic vascular resistance and blood pressure
0 Minimal change in mean blood pressure
• These changes begin early in pregnancy, peak during the 2nd & early 3rd trimester, and
remain relatively constant until delivery
• Cardiac output is increased as early as 5th week due to decreased SVR& increased HR
• Resting pulse rate increases by 10-15 beats per minute (bpm)
• A heart rate >115 bpm may warrant evaluation for pathology

B. Components of Hemodynamic Changes

I INCREASED I DECREASED
Cardiac output (CO) ✓

Stroke volume (SV) ✓

Systemic vascular resistance (SVR) or

✓
total peripheral resistance (TPR)
Plasma (intravascular) volume ✓

Cardiac pre load ✓

Arterial pressure ✓

Brachia! and central systolic pressure ✓

Diastolic pressure ✓

End Diastolic Volume (EDV) ✓

End Systolic volume (ESV) ✓

Resting Pulse (Heart) Rate ✓

Renin ✓

Angiotensinogen ✓

Recall the following formulas:

CO= heartrate(HR)x strokevolume(SY) (BP) = COx TPR
BloodPressure
= (HRx SV)x TPR

25
II.HEART
• As the diaphragm becomes progressively elevated by the uterus in the third trimester,
the heart is displaced to the left & upward and rotated on its long axis
• Apex is moved laterally, producing larger cardiac silhouette in chest radiograph seen in
the latter half of pregnancy

A. Heart Sounds
0 Exaggerated splitting of Sl and increased loudness of both Sl and S2
0 Loud S3
0 Systolic murmur in 90% of gravidas that disappears shortly after delivery
0 Diastolic murmurs are uncommon and may represent pathologic conditions
° Continuous murmurs (mammary souffle) from breast vasculature in 10% of gravidas

B. ECG Changes:
0 Slight left-axis deviation
0 Q waves in leads ll,III and aVF
0 Inverted T-waves in leads Ill, VI-V3

CHANGES IN THE PULMONARY SYSTEM

• Physiological dyspnea (greater awareness of a desire to breathe even in no cardiac/pulmonary
abnormalities exist & does not interfere with normal activity) is common in pregnancy
• It is mainly due to progesterone (and estrogen to a lesser degree)
• Dyspnea is commonly due to upward displacement of the diaphragm (rises by ~4 cm),
manifesting as tachypnea (i.e., acceleration of respiratory rate)

I. THORACIC ANATOMY CHANGES

NONPREGNANT PREGNANT

·"·----+-- Subcostal angle

widens
(68.5° to 103.5°)

Thoracic circumference
increases (+6 cm)

Thoracic diameter
lengthens (+2 cm)

Key Changes
• Diaphragm rises ~4 cm
• The subcostal angle widens appreciably
• The transverse diameter of the thoracic cage lengthens ~2 cm
• The thoracic circumference increases ~6 cm
• The diaphragmatic excursion is greater in pregnant than in non-pregnant women
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition.2018

26
II. LUNGVOLUMES
INCREASED
• lnspiratory capacity (IC)
• Tidal volume (TV)
• Resting minute ventilation
• Peak expiratory flow rates
• Airway conductance
'Functionalresidualcapacity(FRC)= ERV+RV
I DECREASED I UNCHANGED
• Functional residual capacity*
• Respiratory rate
• Expiratory reserve
• Totallung capacity (FRC+ IC)
volume (ERV)
• Lung compliance
• Residual volume (RV)
• Maximumbreathing capacity
• Total lung capacity
• Forcedor timed vital capacity
• Pulmonary resistance

IRV

vc
3200
TLC
TLC 4000
4200
ERV
550
FRC
1350
RV RV
RV 800 800
1000

ff Diaphragm elevation ff
NONPREGNANT TERMPREGNANCY

Lungvolumesare inml
• Most significant changes are reduction in FRC(along with ERV& RV)and increases in IC& TV
• FRC& RVdecreases progressively across pregnancy due to diaphragm elevation
• Enhanced respiratory drive can occur due to stimulatory action of progesterone, low ERV,
and compensated respiratory alkalosis
• 0, delivery in the maternal lungs is increased because of j TV, j hemoglobin mass,
i cardiac output
Source:Cunningham,
FG.Williams
Obstetrics25thEdition.2018
27
-
CHANGES IN THE URINARY SYSTEM
I. OVERVIEWOF THE RENALCHANGES
CHANGES CLINICAL
CORRELATES
• Increases to 1-1.5 cm
Kidney size • Resembles hydronephrosis on • Returns to normal postpartum
sonogram
Renal • GFR& renal plasma flow increase • Increased GFR results in urinary
function by ~50% due to relaxin frequency and nocturia
• Displaced laterally and compressed
at pelvic brim
• Risk for infection due to
Ureter • Ureteral dilatation (right> left) due to
compression
the dextrorotated uterus & cushioning
of the sigmoid colon on the left
• Hyperplasia of bladder muscle
• Urinary incontinence (some) by
elevate the trigone
Bladder 3rd trimester
• Reduced bladder capacity due to
• Risk for infection
uterine compression

II. CHANGESIN RENALFUNCTIONAND URINE

CHANGESINPREGNANCY
Test of Renal Function
-
• Value is usually decreased (i.e.,creatinine clearance is increased ~30%)
Serum
• Creatinine >0.9 mg/dL suggests underlying renal disease that warrants
creatinine
further investigation
Urinalysis II
• May be normal due to increased GFRand impaired renal glucose
Glucosuria reabsorption
• Still warrants investigation for diabetes mellitus
• Protein excretion rate increases to 300 mg/day
• Increases with gestational age
Proteinuria
• Measured using classic dipstick, quantitative 24-hour collection, albumin/
creatinine or protein/creatinine ratio of a single voided urine specimen
• Usually secondary to contamination during urine collection
Hematuria • May be due to UT!
• Common after difficult labor & delivery due to trauma to urethra & bladder

28
;::C=H=A=N=G=E=S==IN=T=H=E==G=A=S=T=R=O=l=N=TE=S=T=l=N=A=L=S=Y=S=T=E I

Key Changes to remember:

• Stomach and intestines are displaced
• Altered mobility of esophagus, stomach, small intestine, colon and biliary tree
• Impaired function of lower esophageal sphincter (LES)
• Decreased gastric acidity
• Altered pancreatic secretion

I. ESOPHAGUS
• "Heart burn or pyrosis" is common in pregnancy due to reflux of acidic secretions into the
lower esophagus from:
0 Altered stomach position
Reduction in LES tone, intraesophageal pressure
Increased intragastric pressure
0 Decreased peristalsis wave speed & amplitude

II. STOMACH
• Gastric a tony (lack of tone)
• Prolonged gastric emptying time
• Stagnation of gastric contents builds up pressure causing gastro-esophageal reflux

III. SMALLINTESTINES,COLON,AND RECTUM

• Decreased motility
• Prolonged intestinal transit time
• Constipation and bloating are common, probably due to hormonal changes that affect motility
• Hemorrhoids are common due to constipation and increased pressure in rectal veins

IV.GALLBLADDER
• Progesterone potentially impairs gallbladder contraction by inhibiting cholecystokinin
(CCK)-mediated smooth muscle stimulation, which is the primary mediator of gallbladder
contraction
• Pregnancy may be associated with an increased risk for gallstones
29
CHANGES IN THE ENDOCRINE SYSTEM
I. PITUITARYGLAND
• Enlarges by approximately 135%
• Due to estrogen-stimulated hypertrophy and hyperplasia of lactotrophs
• May compress optic chiasma & reduce visual fields
PITUITARY
HORMONES I REMARKS

• First trimester: secreted predominantly from the maternal pituitary

Growth hormone
gland, concentrations lie within nonpregnant range
(maternal)
• Serum levels rise slowly at 10 weeks and plateaus after 28 weeks
• Secreted by syncytiotrophoblasts
• As early as 6 weeks AOG:placental GH becomes detectable
Growth hormone • By 20 weeks: placenta becomes the principal source of GH
(placental) • Upregulates insulin-like growth factor-1 (IGF-1 or somatomedin) for
fetal growth; higher levels have been linked to preeclampsia
• Fetal growth still progresses in the complete absence of GH
'
• Functions to ensure lactation
Prolactin • Initiates DNAsynthesis and mitosis of glandular epithelial cells and
presecretory alveolar cells of breast
• Increased production of oxytocin close to term as it is needed for
Oxytocin
uterine contraction

II. THYROIDGLAND
• Hyperplasia and increased vascularity
• Elevation of BMR (basal metabolic rate)
• Pregnancy is a mild hyperthyroid state

A. Thyroid Hormones
THYROID
HORMONES I REMARKS

• Increase in total T3 and T4 hormone levels

T3 and T4 • Unchanged free T3 and T4 hormone levels
• Increase in TBG
Thyrotropin- • Secreted by the hypothalamus
releasing • Do not rise during normal pregnancy but can cross the placenta to
hormone (TRH) stimulate fetal pituitary to secrete TSH
Thyrotropin • Stimulates maternal FT4 secretion
(TSH) • Does not cross the placenta

B. Maternal and Fetal Changes in the Thyroid Glands

INCREASED
• Increased thyroxine-binding globulin
(TBG),hCG----> increased thyroxine (T4) &
triiodothyronine (T3) but free T4 &
free T3 levels are not affected
• FT4 rise slightly and peak with hCG levels
but they return to normal
• Moderate thyroid gland enlargement
due to glandular hyperplasia & greater
vascularity; significant thyromegaly
warrants evaluation
• Increased iodine requirements
I UNCHANGED
• The fetus relies on maternal T4 which
crosses the placenta in small quantities.
• 10-12 weeks: fetal thyroid begins to
concentrate iodine
• 20 weeks: synthesis/secretion of thyroid
hormone by fetal pituitary TSH ensues
• Early exposure to thyroid hormone is
essential for the nervous system

30
III. PARATHYROIDGLANDS

PARATHYROID
HORMONES

Parathyroid
I REMARKS

• Raises extracellular calcium concentrations and lowers phosphate

I
levels; decline in plasma Ca'• or Mg'• stimulates release of PTH
Hormone
(PTH)
• PTH levels decline during the first trimester and rises progressively
throughout pregnancy
• Secreted by the C cells (parafollicular cells) in the thyroid glands;
opposes actions of PTH & Vitamin D
Calcitonin
• Protects maternal skeleton during times of calcium stress
• Calcitonin levels fall during pregnancy and rise postpartum

IV.ADRENALGLANDS (maternal adrenals undergo little morphologic change)

ADRENAL
HORMONES
I DESCRIPTION

• Adrenal secretion not elevated but metabolic clearance rate is decreased

• ACTHand free cortisol levels rise equally as pregnancy progresses
• Theories:
Cortisol 0 Elevated free cortisol in response to elevated progesterone is
needed to maintain homeostasis.
0 Higher free cortisol in preparation for stress of pregnancy, delivery
and lactation
• As early as 15 weeks, maternal adrenal secrete increasing amounts
• Increased renin & angiotensin II, promotes adrenal secretion of
Aldosterone aldosterone
• Protects against natriuretic effect of progesterone and ANP
• May modulates trophoblast growth and placental size

CHANGES IN THE NEUROMUSCULOSKELETAL SYSTEM

I. CENTRALNERVOUSSYSTEM
• Transient pregnancy-related memory decline limited to 3rd trimester
• Intraocular pressure decreases during pregnancy due to greater vitreous outflow
• Krukenberg spindles (brownish opacities on posterior surface of cornea) may be seen
• Difficulty falling asleep, frequent awakening, decreased sleeping time, reduced sleep
efficiency seen after 12 weeks AOG
• Sleep disruption postpartum may contribute to postpartum "blues" or depression

II. MUSCULOSKELETAL SYSTEM

• Progressive lordosis: characteristic feature of normal pregnancy
0 Shift center of gravity back over the lower extremities
0 Sacroiliac, sacrococcygeal, pubic joints: increased mobility
Joint laxity & discomfort does not correlate with levels of estradiol, progesterone or
0

relaxin

31
THE PLACENTA AND UMBILICAL CORD
I. THE NORMAL PLACENTA
• Typical placenta at term weighs 470 g
• Round to oval with a 22 cm diameter & central thickness of 2.5 cm
• Composed of:
Placental disc
0 Extraplacental membranes
0 Three-vessel umbilical cord
• Basal plate: disc surface that lies against the uterine wall which is divided by clefts into
portions (i.e., cotyledons)
• Chorionic plate: fetal surface into which the umbilical cord inserts at the center

II. UMBILICAL CORD

• Most are 40- 70 cm long
• Counting cord vessel number is a standard component of evaluation:
0Embryos initially have two umbilical veins
0In the first trimester, the right vein atrophies to leave one large vein to accompany
two umbilical arteries

III. PLACENTALHORMONES
• Placenta is the main endocrine organ during pregnancy
• Supplies all materials required for fetal growth and energy production, while removing
the products of fetal catabolism (i.e., waste products)
• Secretes several hormones, such as hCG,hPL, estrogen, and progesterone
PLACENTAL
HORMONE I REMARKS

• First key hormone of pregnancy and most important of the placental

peptide hormones
• Used in the early detection of pregnancy in the blood and urine
(pregnancy test)
Human
• Maintains function of corpus luteum beyond 14 days
Chorionic
• Produced almost exclusively in the placenta by the
Gonadotropin
(hCG) syncytiotrophoblasts
• hCGhas thyrotropic activity because it has a similar a-subunit as TSH
0 Stimulates maternal FT4 secretion, leading to transient increase in
FT4 inhibits TSH
0 Inhibits maternal secretion ofTRH and thyrotropin
• Concentrated in syncytiotrophoblasts (5 weeks)
Human Placental
• Maximal concentrations at 34-36 weeks of pregnancy
Lactogen (hPL)
• Plays key roles in fat & carbohydrate metabolism & insulin resistance
• Human pregnancy is a hyperestrogenic state
Estrogen • Syncytiotrophoblast secretes two estrogens: estradiol-17B & estriol
• Promotes growth of the endometrium
• Produced by the syncytiotrophoblast (almost all hormones are
Progesterone produced by the syncytiotrophoblast)
• Facilitates and permits the maintenance of pregnancy

32
FETAL DEVELOPMENT
SECTION
FETAL DEVELOPMENT
FOUR
I
• The moment the ovum is fertilized, the embryonic period starts (conception)
• The first 4 months are critical: any teratogenic effects in this time may cause abortions
and congenital anomalies

I. DEFINITIONOF PERIODS
PERIOD/AGE I DESCRIPTION
• Calculated from the first day of the last normal menstrual period
Gestational or
[LNMP) and is generally used during fetal period, in ultrasound,
Menstrual Age
and in clinical practice
(Age of
Gestation)* • Time elapsed since the first day of the LNMP,a time that precedes
conception
• Time in days or weeks from ovulation
Ovulation or • Ovulation age is used when describing the embryonic period and
Conceptual Age** often, the previable fetal period
• Ovulation age is 2 weeks less than gestational age
'Becausemostwomenknowwhentheirlast periodbegan(butnotwhenovulationoccurred),the timeelapsedsince
the firstdayof the last normalmenstrualperiod(ormenstrualor gestationalage) is usedto determinethe age of
pregnancy.
"The actualembryoor fetalage (i.e.,conceptualage) is the timeelapsedfromfertilizationof the egg near the time
ofovulation.
Source:Cunningham
FG,et al. Williams
Obstetrics.25thedition;2018

IL DEFINITIONOF TERMS
TERM I DESCRIPTION
Embryonic • Time during which organogenesis takes place; begins the third week
Period after LNMP through the eight week
• Corresponds to 7 weeks after fertilization or 9 weeks after the LNMP;
Fetal Period most organ systems have developed, and the fetus enters a period of
growth and maturation
Preterm • A neonate born between 20 weeks up to 37 weeks
Term • A neonate born between 37 weeks up to 42 weeks
Post-term • A neonate born beyond 42 weeks
Infant • Between delivery to 1 year
Source:Cunningham
FG,et al. Williams
Obstetrics.25thedition;2018

33
III. FETAL DEVELOPMENT CHART
• The transition to the fetal period occurs at 7 weeks after fertilization or 9 weeks after the
last normal menstrual period
• A period of growth and maturation

DEVELOPMENTAL
STAGE EMBRYONIC
STAGE FETALSTAGE

Gestationalage
6 7 13 14 20 40
(weeks)
Conceptualage
0 0 2 3 4 5 7 8 9 10 11 12 18 38
(weeks)

••
DEVELOPING
ORGANS

Heart

■
Eyes

• The black bars in the table show the gestational age at which the specific organs or organ
systems are most susceptible to corresponding major congenital abnormalities. The dark
grey bars show the getational age at which the specific organs or organ systems are most
susceptible to functional defects and minor malformations
• The conceptus is termed an embryo at the beginning of the 3rd week after ovulation and
fertilization
• Transition from the embryonic period to the fetal period occurs at 7 weeks after
fertilization, corresponding to 9 weeks after onset of the last menses.

34
;....;A""'M"'-N"'-10"-T"""l...;;;.C....;;.F...;;;;L=U-'-'ID"--------------------I.~ .•
• Amniotic fluid is the liquid that surrounds the fetus after the first few weeks of gestation

I. FUNCTIONS
• Protection of the fetus from ' trauma to the maternal abdomen
• Cushions the umbilical cord from compression
• Antibacterial properties against infection
• Reservoir of fluid & nutrients for the fetus
• Provides necessary fluid and growth factors for fetal development of lungs,
musculoskeletal, ang gastrointestinal systems

II. REGULATION
• Derived almost entirely from the fetus
• Major inputs to the amniotic fluid are fetal urine and fetal lung secretions
• Major physiologic pathway of removal of AF is fetal swallowing and intramembranous
flow (i.e., through skin and fetal membranes)

I SOURCE I REMARKS
Early • Contains same osmolality as
• Maternal plasma as ultrafiltrate
pregnancy maternal plasma
• Transfer of water and small
• Transmembranous flow
molecules across the amnion
• Transfer of water and small
• lntramembranous flow molecules across the fetal vessels on
First half of
the placental surface
pregnancy
• Transfer of water and small
molecules across the fetal skin
• Transcutaneous flow
• Continues until keratinization occurs
at 22-25 weeks
• Produces almost 1 Lat term
• Although fetal urine production
• Fetal urination begins at 8-11 weeks ago of
gestation, it does not become a major
component until 18 weeks AOG
• Produces ·around 350 mL per day;
• Fetal lung fluid secretion half of which is immediately
Late in swallowed
pregnancy
• Resorbs 750 mL per day
• Impaired swallowing secondary
• Fetal swallowing to central nervous anomaly or a
gastrointestinal (GI) obstruction can
result in polyhydramnios
• Intramembranous flow • Resorbs 400 mL per day
• Transmembranous flow • Resorbs minimal fluid

REFERENCES
1. CunninghamFG,LeveneKJ,BloomSL,Dashe JS,HoffmanBL.CaseyBM,SpongCT(Eds.).WilliamsObstetrics.25th edition. New York:McGraw-
Hill Education,2018
2. Curran MA Fetal Development Perinatology.com.Availableonline https://perinatology.com/Reference.AccessedJuly 14, 2021
3. EngleWA;American Academyof Pediatrics Committee on Fetus and Newborn.Agetenninology during the perinatal period. Pediao-ics.2004
Nov;114(5):!362-4.
4. Ross MG,BeallMH.Physiologyof amniotic fluid volume regulation. Uptodate.AccessedJuly 14,2021

35
APPROACH
TOTHE
PATIENT
INOBSTETRICS
 SECTION ONE

_Do_E:_~_:_1:_l~_:w_o_:_:_E_:H_M_:_A_P_P_R_O_A_C_H_T_O_PA_T_I_E_N_T_s_,N_O_
__

I. COMMON TERMINOLOGIES USED

Gravidity: numbir of times that a woman has been pregnant
(irrespective of the outcome)
Nulligravida • A woman who currently is not pregnant & has never been pregnant
Primigravida • A woman who is pregnant for the first time
Multigravida • A woman who has been pregnant more than once
Parity: number of pregnancies that led to a birth '220weeks age of gestation (AOG)
(not by number of fetuses delivered)
Nullipara • A woman who never completed a pregnancy ;,20 weeks gestation
• A woman who has delivered a fetus with an estimated AOGof at least
Primipara
20 weeks
Multipara • A woman who has completed ;,2 pregnancies to "20 weeks AOG
• A woman who has had at least 5 births (live or stillborn) that are at
Grand multipara
least 20 weeks age of gestation

II. GESTATIONALVERSUS OVULATORYAGE

Gestational age
• Calculated from the first day of last menstrual period (see below)
or menstrual age

Ovulatory age or • It is 2 weeks shorter than gestational age

fertilization age • Used by embryologists and other reproductive biologists

III. OBSTETRIC SCORE:GP (T-P-A-L)

• Number of pregnancies, regardless of outcome including current

G Gravidity
pregnancy
p Parity • Number of past pregnancies that reached ;,20 weeks or viability

T Term • Number of term infants delivered ("37 weeks)

p Preterm • Number ofpreterm infants delivered (20-36 6'' weeks)
• Number of abortion/miscarriage ( <20 weeks)
A Abortion
• Ectopic pregnancies as well as molar gestations are included
Live
L babies
• Number ofliving children

39
 Gt 2010 • Preterm • NSD • Live boy, pretenn
G2 2012 • Term • cs • Live girl, term
G3 2014 • 8 weeks • Spontaneous abortion • N/A
• Twin A: live boy
G4 2016 • Preterm • CStwins • Twin B: girl died at age 3 due
to pneumonia
GS 2021 • Current pregnancy
OBScore:G5 P3 (1- 3- 1 - 3)
G - 5 pregnanciesincludingcurrentpregnancy
P - 3 pregnanciesthatreachedbeyond20 weeks(2010,2012,2016)
T - 1 termbabydeliveredin2012
P-3 preterrnbabies:1 deliveredin2010,2 deliveredin2016
A- 1 abortion/miscarriage
thatunderwentD&C
L-3 livechildrencurrently

Example 2: Determine the OB score of a patient with the following OB history, tabulated below:

• Live, term, no feta-maternal

Gt 2012 • Term • NSD
complications
G2 2015 • 8 weeks • Spontaneous abortion • No curettage done
• Primary low transverse • Live,preterm, baby with
G3 2018 • Preterm
CSfor placenta previa congenital heart disease (PDA)

• Tubal pregnancy, • s/p Exploratory laparotomy;

G4 2019 • Unrecalled
right right salpingectomy

GS 2021 • Current pregnancy

OBScore:G5 P2 (1 -1 - 2 - 2)
G - 5 pregnanciesincludingcurrentpregnancy
P - 2 pregnanciesthatreachedbeyond20 weeks(2012and2018)
T - 1 termbabydeliveredin2012
P-1 pretermbabydeliveredin2018
A- 1 abortion/miscarriage
and 1 ectopicpregnancy
L- 2 livechildrencurrently

40
DIAGNOSIS OF PREGNANCY
• Pregnancy is identified when a woman presents any of the following:
Presumptive or diagnostic signs and symptoms

0
Positive home pregnancy test
B-hCG result either urine or blood
Sonographic evidence of pregnancy

PRESUMPTIVE EVIDENCE I PROBABLE EVIDENCE I POSITIVE

• Nausea, vomiting
• Urinary frequency /urgency
V)
:;: • Quickening (fetal movement
0 perceived by the mother):
E- ° For primigravids: occurs
Q.
:;: at 18-20 weeks AOG
>-
V)
° For multigravids: occurs
at 16-18 weeks AOG
• Breast enlargement
• Amenorrhea (a delay >10
days from expected menses
is highly suggestive)
EVIDENCE
II .
• Abdominal distention
• Braxton-Hicks
contractions: painless,
irregular contractions
which may be both --·
palpable and visible
• Positive pregnancy test • Fetal heart tone
• Abdominal enlargement , 5 wks: TVS
• Outlining of fetal parts 0 10 wks: Doppler

• Chadwick sign (6 weeks): • Hegar sign (6-8 weeks): , 16 wks:

vaginal mucosa appears
dark bluish red & congested
• Chloasma or melasma
V) gravidarum (mask of
;z pregnancy)
"'
vi • Linea nigra ( discoloration of
linea alba)
• Striae gravidarum ( stretch
marks)
• Spider telangiectasia
• Breast changes (broad
areola, tenderness,
colostrum expressed)
• Thermal changes
"PRESUME"
• Period absent (amenorrhea)
• Really tired (fatigue)
• Enlarged breast
• Sore breast
V)
• Urination increased
~ • Movement of fetus in uterus
;z • Emesis and nausea
0 • A softening of cervix
~
""
;z
::;:
TVS:transvaginalsonography(ultrasonography)
AOG:age of gestation
FHT:fetalhearttones (fetalheart sounds)
softening of isthmus auscultation
• Goodell sign ( 4 weeks): • Perception of fetal
softening of cervix movement by
( consistency of cervical examiner
tissue is similar to that of • Ultrasound evidence
the lips of the mouth)
• Ballottement: bouncing
back of fetus against
fingers when uterus is
pushed during palpation
"PROBABLE" "FETUS"
• Positive pregnancy test • Fetal movements felt
• Returning of the fetus: by doctor or nurse
"external ballottement • Electronic device
• Outline of fetus can be detects FHT
palpated • The delivery of baby
• Braxton Hicks • Ultrasound detects
Contractions the fetus
• See visible
• Bluish color of vulva, movement of the
cervix, vagina (Goodell baby by the doctor
sign) or nurse
• Lower uterine segment
(LUS) becomes soft
(Hegar Sign)
• Enlarged uterus

Source:https://www.registerednursern.com/signs-of-pregnancy-presumptive-probable-positive/

41
PREGNANCY TESTS
I. HUMAN CHORIONIC GONADOTROPHIN (p-hCG)
• Basis for endocrine assays of pregnancy
• Syncytiotrophoblast produce P-hCG in amounts that increase exponentially during the
first trimester following implantation
• Main function is to prevent involution of the corpus luteum (principal site of
progesterone formation during first 6 weeks of pregnancy)

A. Biochemistry of hCG
• Glycoprotein with high carbohydrate content
• Heterodimer composed of two subunits: alpha and beta
• Alpha-subunit: identical to LH, FSH, and TSH
• Beta-subunit: used as a basis for pregnancy detection

B. P-hCG Detection
• Detected in maternal serum or urine by 8 to 9 days after ovulation
• In normal pregnancy, the serum hCG "doubles" its level of concentration every 1.4 to
2.0 days and reaches peak levels at 60-70 days
• Not observed in cases of miscarriages, ectopic pregnancies, or molar gestations
• Concentration declines slowly until a nadir at approximately 18-20 weeks

E t d /3hCGL I . P , (Th RG t· St d )
GESTATIONAL
AGE
I MEDIAN {RANGE) I GESTATIONAL
AGE
I MEDIAN (RANGE)

<9weeksAOG 59,973 (455 - 142,584) 16weeksAOG 29,614 (7,512 - 132,084)

9weeksAOG 75,494 (22,655 - 129,909) 17weeksAOG 24,426 (5,637 - 151,558)
lOweeksAOG 74,655 (16,080 - 163,393) 18weeksAOG 20,693 (3,822 - 75,993)
11 weeksAOG 62,493 (10,340 - 187,852) 19weeksAOG 17,609 (3,895 - 90.628)
12weeksAOG 56,004 (8,105 - 164,125) 20weeksAOG 17,354 (3,128 - 78,841)
13 weeksAOG 52,377 (4,618 - 166,478) 21 weeksAOG 15,088 (1,542 - 73,485)
14weeksAOG 47,267 (5,925 - 144,054) 22weeksAOG 16,174 (2,559 - 86,541)
lSweeksAOG 37,303 (4,834 - 122,037) 23 weeksAOG 12,415 (1,957 - 65,192)
Korevaaret al. TheR Generation
Study,2015

Sample Case: A patient with amenorrhea for 8 weeks

• At 8 weeks AOG,P-hCG is expected to be within the range of 455 - 142,584 IU/L and already
with fetal cardiac activity.
• If on ultrasound, no gestational sac is seen and P-hCG is only 750 IU/mL, a repeat P-hCG may
be requested after 2 days to establish fetal viability.
• If pregnancy is viable, we expect ~-hCG to be 1500 IU/mL.
• A decreasing ~-hCG or less than Zx increase from baseline points to a non-viable pregnancy.
C. Other Causes of Elevated hCG or Positive Assays:
• Heterophilic antibodies that bind to animal-derived test antibodies in an immunoassay
0 Molar pregnancy or gestational trophoblastic neoplasia (GTN)
• Exogenous hCG injection for weight loss
• Renal failure with impaired hCG clearance
• Physiological pituitary hCG
• hCG-producing tumors from GI, ovary, bladder or lung

II. ULTRASOUND RECOGNITION

• Transvaginal ultrasound (TVS): commonly used to accurately establish gestational age,
confirm viability, and locate pregnancy

A. Gestational Sac
• Small anechoic fluid collection within the endometrial cavity
• The first sonographic evidence of pregnancy
• Seen with TVS by 4 to 5 weeks gestation
• Implants eccentrically in the endometrium
42
B. Potential Indicators of Early Intrauterine Pregnancy:
0 lntradecidual sign: anechoic center surrounded by a single echogenic rim; OR
0 Double decidual sign: two concentric echogenic rings surrounding the gestational sac:

I
decidua parietalis and decidua capsularis

.
~·~, A Fetal pole
B Yolk sac

:~·,
:j,)#• C
D
E
Gestational sac
Decidua capsularis
Decidua parietalis

• Yolk sac: brightly echogenic ring with an anechoic center (confirms an intrauterine
location for the pregnancy and seen by middle of 5th week)
• Embryo: >6 weeks, linear structure adjacent to yolk sac, cardiac motion noted at this point
• Double decidual sign: (1) decidua capsularis (inner), (2) decidua parietalis (outer)
• Crown-rump length (CRL): up to 12 weeks AOG, predictive of gestational age within 4 days

C. Gestational Sac versus Pseudogestational Sac

0Gestational sac: evidence of a normal intrauterine pregnancy
0Sonologic features of a pseudogestational sac: seen in cases of ectopic pregnancy
which warrant investigation of the adnexa during ultrasound

GESTATIONAL SAC I PSEUDOGESTATIONAL SAC

(PSEUDOSAC)
• Small anechoic fluid collection within the endometrial cavity
• First sonographic evidence of pregnancy
• Implants eccentrically in endometrium • Seen in the midline of endometrial cavity
• Presence of the double decidual sign • Absence of the double decidual sign
• Seen with ectopic pregnancy

D. Indications & Components of Standard Ultrasound by Trimester

FIRST TRIMESTER
• Gestational sac size, location and number;
embryo and/or yolk sac determination:
confirm an intrauterine pregnancy, evaluate
a suspected ectopic pregnancy
• Crown-rump length: estimate AOG
• Fetal number, including amnionicity and
chorionicity of multifetal gestations:
diagnose or evaluate multifetal gestations
• Fetal activity: confirm cardiac activity
• Assessment of embryonic/fetal anatomy
appropriate for the first trimester
• Evaluation of the maternal uterus, adnexa,
and cul-de-sac: evaluate pelvic pain,
maternal pelvic masses and/or uterine
abnormalities, and define the cause of
vaginal bleeding
• Evaluation of fetal nuchal region, with
assessment of fetal nuchal translucency
• Assess for certain fetal anomalies, such as
anencephaly, in high risk patients
Source: The Americanlnstituleof Ultrasoundin Medicine,2013a; Cited in WilliamsObstetrics25th Edition
43
I SECOND & THIRD TRIMESTER
• Fetal number, including amnionicity and
chorionicity of multi fetal gestations
• Fetal cardiac activity
• Fetal presentation
• Placental location, appearance and
relationship to the internal cervical os, with
documentation of placental cord insertion
site when technically possible
• Amniotic fluid volume
• Gestational age assessment
• Fetal weight estimation
• Fetal anatomic survey, including
documentation of technical limitations
• Evaluation of the maternal uterus, adnexa,
and cervix when appropriate
 SECTION TWO
PRECONCEPTIONAL CARE

OVERVIEW OF PRECONCEPTIONAL CARE

It is a set of interventions that aim to identify & modify biomedical, behavioral and social
risks to woman's health or pregnancy outcome through prevention and management

I. OBJECTIVES
OF PRECONCEPTIONAL
CARE
• Improve knowledge, attitudes, & behaviors related preconceptional health
• Assure that all women of childbearing age receive preconceptional care services
(including evidence-based risk screening, health promotion, & interventions) that will
enable them to enter pregnancy in optimal health
• Reduce risks indicated by a previous adverse pregnancy outcome through
interconceptional interventions to prevent or minimize recurrent adverse outcome
• Reduce the disparities in adverse pregnancy outcomes
Source:ACOG;2017and SMFM;2014

II. THE COUNSELINGSESSION

• Gynecologists, internists, and pediatricians have the best opportunity to provide
preventive counseling during periodic health maintenance examinations
• Counselors should be knowledgeable regarding relevant medical diseases, prior surgery,
reproductive disorders, or genetic conditions and must be able to interpret data and
recommendations provided by other specialists
• Intake evaluation should include a thorough review of medical, obstetrical, social, and
family histories

COMPONENTS OF PRECONCEPTIONAL CARE

I. PARENTALAGE
• Adolescent pregnancy (15-19 years old)
• Most pregnancies are unplanned.
• Increased risk for anemia, preterm delivery, preeclampsia and STD
• Pregnancy after 35 years old:
• Increased risk for obstetrical complications
• Maternal mortality rate is higher for those >35 years old
• Maternal age-related risks primarily stem from:
Maternal • Indicated preterm delivery for maternal complications (e.g.,
Age hypertension, diabetes)
• Spontaneous preterm delivery
• Fetal growth disorders related to chronic maternal disease or
multifetal gestation (increased dizygotic twinning)
• Fetal aneuploidy
• Pregnancies resulting from use of assisted reproductive technology (ART):
associated with obstetrical morbidities (e.g., preterm delivery from
multifetal pregnancy, placenta previa, abruptio, preeclampsia, and risk for
malformations from intracytoplasmic sperm injection [lCSI])
• Possible link between increasing paternal age and complex neuropsychiatric
Paternal conditions
Age • Increased incidence in older men of genetic diseases in offspring caused by
new autosomal-dominant mutations

44
II. MEDICALHISTORY
• General points include how pregnancy will affect maternal health and how a high-risk
condition might affect the fetus

COM ORB IDS

Diabetes
mellitus
I REMARKS ;

• Maternal & fetal pathology is associated with hyperglycemia

• Goal is to have the lowest HBAlc level possible without undue hypoglycemic
risk to the mother
• Investigate for related complications and end-organ damage
• Increased risk of macrosomia, and congenital anomalies (CNSdefects, brain
I
.

and spinal defects, and caudal regression syndrome)

• Treatment goals attempt to achieve seizure control with monotherapy and
with medications considered less teratogenic
• Folic acid 4 mg supplementation reduces risk of congenital abnormalities
from those exposed to carbamazepine, phenobarbital, phenytoin and
primidone
Epilepsy
• Criteria to discontinue anti-seizure medications before pregnancy:
• Seizure-free for 2-5 years
• Single seizure type
• Normal neurological examination & normal intelligence
• Normalized EEGwith treatment
• Discuss situations in which pregnancy is contraindicated
Cardiovascular
• Discuss medication teratogenicity (e.g., warfarin, ACEinhibitor, ARB) and
disease
switch to less dangerous agents when conception is planned
• Assess those for end-organ damage from hypertension
Chronic
• Optimize blood pressure (BP) control
hypertension
• Select or switch to an agent appropriate for pregnancy
• Optimize pulmonary function
Asthma
• Treat women with pharmacologic step therapy for chronic asthma
• Optimize BP control before conception
Renal disease • Counsel women taking ACEinhibitors and ARBs about teratogenicity and
the need to switch agents before pregnancy
Thyroid • Ensure iodine-sufficient diet
disease • Treat overt hyper- or hypothyroidism
• Commonly encountered CTD's include rheumatoid arthritis (RA) and
systemic lupus erythematosus (SLE)
Connective
• Counsel on flare risk during/after pregnancy
tissue disease
• Discuss teratogenicity of drugs (e.g., methotrexate and leflunomide for RA or
(CTDs)
mycophenolate mofetil and cyclophosphamide for SLE)
• Stop NSAIDsby 2 7 weeks' gestation
• Screen for symptoms of depression
Psychiatric
• Counsel on risks of treatment and of untreated illness and the high risk of
disorders
exacerbation during pregnancy and the puerperium
Dermatological • Discuss isotretinoin and etretinate teratogenicity and effective
disease contraception during their use
• Immunization during pregnancy with toxoids (e.g., tetanus) or
killed bacteria or viruses (e.g., influenza, pneumococcus, hepatitis B,
meningococcus, and rabies) and COVID-19vaccine are not contraindicated.
Immunizations
• Live-virus vaccines (e.g., varicella-zoster, MMR,polio, and yellow fever) are
contraindicated during pregnancy(> 1 month should ideally pass between
vaccination and conception attempts]

Source:Cunningham,
FG.WilliamsObstetrics25thEdition;2018
American Academyof Neurology;2005
POGSPracticeBulletinNo.1,ThirdUpdate,August2021

45
III. GENETICDISEASES
• Congenital conditions that clearly benefit from patient education include neural-tube defects
(NTDs), phenylketonuria (PKU), thalassemia and other common genetic diseases
• Pedigree construction is the most thorough method for obtaining a family history as a
part of genetic screening
• Health and reproductive status of each "blood relative" reviewed for medical illnesses,
mental retardation, birth defects, infertility, and pregnancy loss

GENETIC
DISEASE
I REMARKS

• Second most frequent structural fetal malformation (most frequent

are cardiac anomalies J
Neural tube • Preconceptional folic acid therapy significantly reduced the risk for
defects (NTDs) recurrent NTD
• Recommended folic acid 400-800 ug daily before conception and
through the first trimester
• Inborn error of phenylalanine metabolism carried by the mother
• Advice mothers with PKU to adhere to a phenylalanine-restricted diet
before pregnancy
Phenylketonuria
• Phenylalanine crosses the placenta & damage developing fetal organs
(PKU)
• Fetal complications from women with untreated PKU: mental
retardation (most common}, microcephaly, fetal growth restriction,
spontaneous abortion, and congenital heart disease
• Disorders of globin-chain synthesis are the most common single-gene
disorders worldwide
• Maternal thalassemia is a common cause of anemia during pregnancy
• Screen partners of women with known thalassemia, because if the
Thalassemias
partner is also a thalassemia trait carrier, then the risk of the baby
inheriting the disease also increases
• Homozygous alpha thalassemia in the baby often results in fatal
hydrops fetalis

IV.REPRODUCTIVEHISTORY
• Information should be sought regarding the following:
0 Infertility
0 Abnormal pregnancy outcome: miscarriage, ectopic pregnancy & recurrent pregnancy loss
0 Obstetrical complications: cesarean delivery, preeclampsia, placental abruption &
preterm delivery
0 Identification of a genetic abnormality in stillbirth

46
V.SOCIALHISTORY
A. Alcohol Intake
CONDITION I CRITERIA

Documented
Prenatal Alcohol
Exposure
• One or more required:
• ~6 drinks per week for ~2 weeks
0

0
~3 drinks per occasion for ~2 occasions
Risk identified with a validated screening questionnaire
Laboratory testing indicating alcohol intoxication or positive
alcohol-exposure biomarker
I
.

0 Documentation of an alcohol-related legal or social problem

• All are required:
0 Dysmorphic facial features (~2 required):
• Short palpebral fissures
• Thin vermilion border of the upper lip
0 Smooth philtrum
0 Prenatal and/or postnatal growth impairment, slOth percentile
Fetal Alcohol
0 Abnormal brain growth, morphogenesis, or physiology(~1 required):
Syndrome • Head circumference sl0th percentile
0 Structural brain abnormalities
0 Recurrent nonfebrile seizures
0 Neurobehavioral impairment (defined as >1.5 SD below mean):
° Child <3 years: developmental delay
° Child ~3 years: global cognitive impairment, or cognitive
deficit in at least 1 neurobehavioral domain, or behavioral
deficit in at least 1 domain
Source:BertrandJ; et al. MMWRRecommRep;2005
HoymeHE,et al. Pediatrics;2005

B.Smoking
• Affects the fetus in a dose dependent manner
• Increases risk of preterm labor, fetal growth restriction, and low birthweight
0Associated with increased risk for attention-deficit/hyperactivity disorder (ADHD)
and behavioral and learning problems
0Increases risk for uteroplacental insufficiency and placental abruption

C. Environmental Exposures
0 Infections: Cytomegalovirus, Respiratory Syncitial virus, Parvovirus, Rubella
• Heavy metals & organic solvents (e.g., industrial workers)
0 Pesticide & contaminated well water (e.g., women in rural areas)

D.Diet
• Craving for and consumption of ice, laundry starch, clay, dirt or
other non-food items
Pica • Should be discouraged due to its inherent replacement of healthy
food with nutritionally empty products
• Considered to be triggered by iron deficiency in some women
• Encourage intake of protein-rich food: egg, cheese, soy, legumes,
Vegetarian diets
etc.
• Associated with preeclampsia, gestational diabetes, labor
Obesity
abnormalities, cesarean delivery and operative complications
• Increase maternal risk of nutritional deficiencies, electrolyte
Anorexia and disturbances, cardiac arrhythmias and gastrointestinal pathology
bulimia • Greater risk of low-birthweight, small head circumference,
microcephaly, and small for gestational age

47
E. Recreational Drugs
DRUG I FEATURES AND EFFECTS
• Small-for-gestational age, hypertensive complications, placental
Amphetamines
abruption, preterm birth, stillbirth, behavioral abnormalities
• Maternal effects: cerebrovascular hemorrhage, myocardial damage,
and placental abruption
Cocaine • Fetal effects: cleft palate, cardiovascular abnormalities, urinary tract
anomalies, fetal-growth restriction, preterm delivery, behavioral
abnormalities and cognitive impairments
• Spina bifida, gastroschisis, cardiac abnormalities with
Opioids- periconceptional opioid exposure
Narcotics • Heroin addiction is associated with preterm birth, placental
abruption, fetal-growth restriction, and fetal death
• Cannabinoids are not considered to be major teratogens, but may
Marijuana
disrupt normal fetal brain development
Phencyclidine • Not associated with congenital anomalies
(PCP) or angel • Newborns experience withdrawal symptoms (e.g., tremors,
dust jitteriness, and irritability)
• Common solvent used in paints and glue
• Toluene embryopathy is phenotypically similar to fetal alcohol
Toluene syndrome
• Pre- & postnatal growth deficiency, microcephaly, midface hypoplasia,
short palpebral fissures, wide nasal bridge, & developmental delays
• Contains a complex mixture of nicotine, cotinine, cyanide, thiocyanate,
carbon monoxide, cadmium, lead, and various hydrocarbons
• Fetotoxic and may have vasoactive effects or reduced oxygen levels
• Associated with cardiac anomalies (dose-related), hydrocephaly,
Tobacco
microcephaly, omphalocele, gastroschisis, cleft lip and palate, and
hand abnormalities
• Electronic nicotine delivery systems have adverse effects on fetal
brain and lung development
Source:StillermanKP.et al. ReprodSci;2008
ACOG;2017

F.Intimate Partner Violence (IPV)

0 Pregnancy can exacerbate interpersonal problems and is a time of elevated risk from
an abusive partner
0 lPV associated with increased risk for hypertension, vaginal bleeding, hyperemesis,
preterm delivery, and low-birthweight infants, homicide

48
 SECTION
PRENATAL CARE
_O_V_E_R_V_IE_W_O_F_P_R_E_N_A_I_'A_L_C_A_R_E
__ -_-_-_-_-_-_-_-_·-_-_
THREE

..._-_-_-_-_-_-_-_-_-_-_-_-•
• Prenatal care refers to healthcare provided to a woman during pregnancy
I
• It refers to early and ongoing risk assessment to prevent, recognize, and treat conditions
associated with maternal and neonatal morbidity and mortality
• Refers to a series of clinical visits and ancillary services designed to promote the health
and well-being of the mother, fetus, and family

I. GOALSOF PRENATALCARE
• It should provide opportunities for the following:
Physician and patient to be better acquainted
0 Learn something about the patient's emotional attitude toward pregnancy and labor
Instruction for the patient and her husband in optimal care for herself & the coming baby
Optimal instruction of the patient and her husband in a prepared childbirth program

II. SCHEDULEOF PRENATALVISITS

PROFILE
I SCHEDULE OF VISITS*
• Every 4 weeks until 28 weeks AOG
Traditional • Every 2 weeks from 28 until 36 weeks AOG
• Every week from 36 weeks AOGuntil term
High-risk • Complicated pregnancies may require return visits at 1- to 2- week intervals
'WHOsuggeststhe following
visits:oncein 1sttrimesterto screenforriskfactors.then at 26, 32. &38 weeks
Source:Cunningham, FG.Williams Obstetrics25thEdition.2018
AAP&ACOG,2017
Lu,M.Encyclopedia
of Infantand EarlyChildhoodDevelopment; 2008

III. OVERVIEWOF THE COMPONENTSOF ROUTINEPRENATALCARE

COMPONENT 'FIRST~
VISIT

History
Complete history ✓

Updated history ✓ ✓ ✓

PhysicalExam -
Complete examination ✓

Blood pressure ✓ ✓ ✓ ✓

Maternal weight ✓ ✓ ✓ ✓

Pelvic/cervical exam ✓ ✓'

Fundal height ✓ ✓ ✓ ✓

Fetal heart rate (FHR) & fetal position ✓ ✓ ✓ ✓

'Pelvicand cervicalexamis perfonmed

weeklyslarting37 weeksAOG

49
IV.OVERVIEWOF THE COMPONENTS OF ROUTINE PRENATALLABORATORYTESTS

Complete blood count

COMPONENT
I FIRST~
VISIT

✓ ✓

Blood Type and Rh Factor ✓

Antibody screen ✓ A

Pap smear ✓

Fasting Blood Sugar 1 ✓

Oral Glucose Tolerance Test (OGTT)1 ✓

Fetal aneuploidy screening 2 B B

Neural tube defect screening B

Urine protein assessment ✓

Urine culture 3 ✓

Rubella serology ✓

Syphilis serology ✓ C

Gonococcal screening D D

Chlamydia! screening ✓ C

Hepatitis B serology ✓ D

HIVserology B D

Group B streptococcus culture E

Tuberculosis screening•
Preeclampsia screening 5 F
A Pertormat28weeks
BTestshouldbeoffered
C High-risk
women shouldberetested
atthebeginningofthethirdtrimester
D High-risk
women shouldbescreenedatthefirstprenatal
visitagaininthethirdtrimester
E Rectovaginal
culture
should
beobtainedbetween 35to37weeks
F Pertorm
at11to13617weeks

1 Filipinoshavea higherriskof developing overtOMandgestationaldiabetesmellitus(GDM).Screeningfor GDM

shouldbe startedduringthe first prenatalconsultwithobtainingfastingbloodsugar(FBS)
2 Firsttrimesteraneuploidyscreeningmaybe offeredbetween11and 14weeks
3 In the absenceof facilitiesfor urineculture,significantpyuria(>10 wbc/hpnor a positivegramstain
(>2 microorganisms/hpn in twoconsecutivemidstreamurinesamplescan be usedto screenfor asymptomatic
bacteriuria
4 Screeningcan be donewitheitherMantouxtuberculintestor a tuberculosis
bloodtest as indicatedat anyvisit

5 Allpregnant
women should
bescreenedforearlypreecampsia
usingmaternal
riskfactors,
maternal
uterine
arteryevaluation,
and
serumbiomarkers growth
[placental factor(PIGF)
andpregnancy-associated
plasma protein
A (PAIPP-A))
Source:Cunningham.FG.WilliamsObstetrics25thEdition.2018
POGSCPGon GestationalDiabetesMellitus,2018
PhilippineCPGon the Diagnosisand Management
of UTIin Adults;2015

50
INITIAL PRENATAL EVALUATION
• Major goals include:
Define the health status of the mother and fetus
• Estimate the gestational age
• Initiate a plan for continuing obstetrical care

I. PREVIOUSAND CURRENTHEALTHSTATUS
COMPONENT I
• Name, age, status
REMARKS
I
.

General data • Gravidity, parity, OB-score

• Address, occupation, date of admission/ consultation
• Prenatal check-up is the most common reason
Chief
• Complaints may be gynecological, surgical, or even problems
complaint
unrelated to pregnancy
• Regardless of the reason for consult, the following should be present
in the HPI:
• Last normal menstrual period (LNMP)
History of • Previous menstrual period (PMP)
present illness • Expected date of delivery (EDD)/ confinement (EDC)
(HP!) • Age of gestation (AOG)
• Quickening
• Morning sickness
, Signs & symptoms
• Medical disorder: allergies, cardiac disease, DM, epilepsy, exposure
to rubella, gonorrhea, hepatitis, hypertension, immunizations, renal
diseases, urinary tract infection, thyroid disorder, tuberculosis,
Past medical
hypercoagulability states from lupus anticoagulant or anticardiolipin
history
antibodies, mental health disorders, HIV,STDs, abnormal pap smears
• Medication history
• Surgical history
• Smoking (pack years)
• Alcohol intake
Social history
• Occupation, environmental exposures, hobbies & recreational activities
• Use of illicit drugs
• History of multifetal gestations
Family history • Hereditary diseases (e.g., asthma, cancer, DM, heart disease)
• Congenital anomalies

51
II. OBSTETRICAND GYNECOLOGICAL
HISTORY
COMPONENT I REMARKS
• Last normal menstrual period (LNMP)
Menstrual
• Previous menstrual period (PMP)
history
• Presence of associated pain (dysmenorrhea, Mittelschmerz)
Contraceptive • Failure of current method
use • Previous methods, including complications, reasons discontinue
Cervical • Most recent Pap smear result
and vaginal • History of abnormal Pap smear: nature of diagnosis, treatment, and
cytology follow-up
• History of sexually transmitted infections
Infections • History ofvaginitis, including types, frequency, and treatment
• History of pelvic inflammatory disease
Fertility/ • Difficulty in conceiving in the past
infertility • Prior fertility evaluation and treatment
• Presence of sexual activity
• Types of relationships
Sexual history
• History of dyspareunia
• Sexual dysfunction of both patient and partner
• Describe each pregnancy and the outcome.
• Describe any maternal, fetal, or neonatal complications
Obstetrical
• 08 Score is expressed with Gravidity, Parity followed by (Ierm -
history
£reterm -Abortion - Living children)
• History of antenatal visits: place and how many visits

III. DANGERSIGNSOF PREGNANCY

DANGER SIGN I POSSIBLE CAUSES
• Pyelonephritis
Fever and chills
• Intra-amniotic infection
Persistent vomiting • Hyperemesis gravidarum
Dysuria • Urinary tract infection
Swelling of face and fingers • Severe preeclampsia
Severe & persistent headache • Severe preeclampsia
Blurring of vision • Severe preeclampsia
• Placenta previa
• Placenta abruption
Vaginal bleeding
• Abortion, hydatidiform mole, or ectopic pregnancy
• Preterm labor
• Preterm labor
Abdominal pain/cramping
• Severe preeclampsia
Fluid leakage from vagina • Rupture of fetal membrane
Change in frequency/intensity of
• Fetal compromise
fetal movements

52
IV. GENERAL PHYSICAL EXAMINATION*
Vital signs & • Blood pressure, pulse and hea1t rate, temperature, respiratmy rate
general survey • Height and weight

HEENT

Breasts
• Conjunctiva for pallor (or signs ofanemia)
• Physiologic enlargement of the thyroid gland in pregnancy
• Chloasma or melasma ("mask of pregnancy": darkening of the face)
• Check for breast symmetry or skin retractions in the breast
• While patient is sitting up, examine the axilla & area above clavicle
I
.
for lymphadenopathy
• Ask patient to lie down and palpate the breasts
Lungs • Check for adventitious breath sounds
• Because of the enlarging abdomen, the apex beat changes in location
(lateral and upwards)
• Normal changes in heart sounds:
0 Exaggerated splitting of S1
0 No change in S2

Heart 0 S3 gallop may be present

0 Systolic ejection murmur along the left sternal border from

increased flow across the aortic and pulmonic valves
0 Diastolic murmurs are always pathologic
0 Mammary souffle: "puff of air" or venous hum from increased

blood flow in the breast vasculature

Extremities • Check for edema or varicosities
• Integrity of the perineum
Rectal and
• Masses in cul de sac, uterine wall, uterosacral ligaments
rectovaginal
• Parametria
exam
• Presence of hemorrhoids
•Abdominaland pelvicexaminationare discussedbelowin detail

V. ABDOMINAL EXAMINATION
A. Listening to the Fetal Heart Tone (FHT)
0 Locate where the fetal tone is heard best
0 Best place to locate the heart tone is along the fetal back
° Fetal heart rate (FHR): normally 110-160 beats per minute (bpm) with 10-15 bpm
variability from second to second
0 Inability to hear fetal heart sound should be investigated with formal ultrasound

Detecting Fetal Heart Tones

AOG I METHOD
5-6weeks • Detectable by transvaginal sonography
10 weeks • Can be heard via Doppler ultrasound
16weeks • Earliest that can be heard with a standard non amplified stethoscope
20 weeks • Audible by stethoscope in 80% of women
22 weeks • Audible by stethoscope in all women
Source:Cunningham,FG.WilliamsObstetrics25th Edition.2018

53
Measuring the Fundal/Fundic Height
0 Measured along abdominal wall from the top of the symphysis pubis to the top of the fund us
0 Bladder must be emptied before fundal measurement
0 Between 20 and 34 weeks gestation, the height of the uterine fund us measured in
centimeters correlates closely with gestational age in weeks (e.g., at 28 weeks, the
fundic height is expected to be 28 cm)

Step 1: Palpate the fund us of the uterus prior to placement of the tape measure

~
,_-w,,>---'~
~~
~
Walk fingers up along Find the fundus Curve fingers
the side of the abdomen (hard ball under skin) into the belly

Step 2: Placement of the tape measure.

Fundus
(if not mid line, • Tape measure
may adjust uterus to midline) Fund us may be placed
on the midline

r~_o:~i:hysis
t~_'\@ of the abdomen
as long as the

'~~~~.
uterus is gently
pushed to the
~l
\W,j, ~
midline to obtain
the fundal height

Fundic Height Correlated with Age of Gestation (AOG)

AOG
I HEIGHT OF THE FUNDUS*
12 weeks • Uterus felt above the pubic symphysis
16weeks • Midway between umbilicus and pubic symphysis
20-ZZweeks • At the level of umbilicus
28weeks • Between umbilicus and xiphoid process
40weeks • Fundic height decreases (because the fetal head enters the pelvic cavity)
'The measurementof fundicheightis used to monitorfetal growthand amnioticfluidvolume.
Source: Cunningham,FG. WilliamsObstetrics25th Edition.2018

54
C. Performing the Leopold Maneuvers (LM)
• Fetus can usually be palpated through the anterior abdominal and uterine walls
• Leopold maneuvers determine the fetal position

I
° Findings provide information about the presentation and position of the fetus and the
extent to which the presenting part has descended into the pelvis

LEOPOLD MANEUVER* I OBJECTIVE I REMARKS .

• Which fetal pole occupies
thefundus? • Cephalic presentation: the
0 0 • Examiner palpates the breech (buttocks) is in the

~
fund us with the tips of the
fingers of both hands
1 • Examiner palpates fundal
area & distinguishes between
the irregular, nodular breech
[buttocks) versus the round
mobile and ballotable head
fund us (large, nodular mass
in the fundus)
• Breech presentation: the
head [hard and round
ballotable head) is in the
fund us

• Fetal back is a hard, resistant

• Where is the fetal back? convex structure. It is where
• Palms of examiner are fetal heart is best heard.
2 'v· I placed on either side of the • Fetal extremities are
abdomen [Umbilical grip) numerous, small, irregular,
> and mobile parts
.,

• Fetal head is engaged: mass

• What fetal part lies above
is not moveable (e.g., it is
the pelvic inlet?
fixed)
• Examiner grasps the lower
3
) portion of abdomen above
the symphysis pubis (Pawlick
• Fetal head is not engaged: a
moveable (ballotable) mass
is felt, which can be displaced
> grip)
upward

• Head is flexed if cephalic

• Which side is the cephalic
prominence is on the same
prominence on? Is the head
side with the small parts
extended or flexed? Isfetus in
(presenting part is the vertex)
the correct fetal attitude?
• Head is extended if cephalic
• Done if fetal head is engaged
prominence is in the same side
& if cephalic prominence has
4 not been identified yet
with the fetal back (presenting
' part is the face)
• Examiner faces patient's feet
• If head is engaged in the pelvis,
& places one hand each on
examiner's hands will diverge
either side of the lower pole
• If head is not engaged in
of the uterus just above the
the pelvis, both hands will
inlet (Pelvic grip)
converge Qoin together)
'First threemaneuvers
are donewiththeexaminerfacingthe patient'shead;thefinalmaneuveris donewiththe
examinerfacingthe patient'sfeet
Source:Cunningham,
FG.WilliamsObstetrics25thEdition.2018

55
 Example: Left Anterior Occiput. The occiput (posterior fontanel) is facing the left abdominal
side of the mother and near the pubis symphysis (anterior)
LMl: breech LM2: fetal back on LM3: maybe LM4: cephalic
(buttocks) occupies mother's left side engaged or not prominence on right
the fundus

~
VI. PELVICEXAMINATION
~N(~) ~
• A pelvic examination is performed with special attention to the uterine size & adnexa
• In late pregnancy, vaginal examination often provides valuable information:
° Confirmation of the presenting part and its station
° Clinical estimation of pelvic capacity and its general configuration
Amnionic fluid volume adequacy
Cervical consistency, effacement, and dilatation
External • Look for lesions and swellings
genitalia • Discoloration of skin
• Vagina:
• Assess for vaginal discharge, anomalies (e.g., septum), and masses
• Chadwick sign: violaceous discoloration due to increased blood flow
Speculum • Cervix:
examination • Bluish-red passive hyperemia of the cervix may be noted in pregnancy
• Nabothian cysts may be prominent
• Pap smear may be done and specimen obtained to check for Chlamydia and
Neisseria gonorrhea, if indicated

Internal efaminatto~f,Bima~ual Examination

• Describe size, configuration of external os, & abnormalities ( e.g., pain in motion,
ulcers, masses)
• Goodell sign: softening of the cervix
Cervix
• Hegar sign: softening of the isthmus
• Lesions of cervix, vagina or vulva should be evaluated as needed by colposcopy,
biopsy, culture or dark-field examination.
• Changes in pregnant uterus, mobility & position, and size & configuration
• Gestational age assessment: uterine size correlation of gestational age
• When uterine size differs from the predicted age of gestation, sonographic
Corpus
assessment if warranted
• Causes of discrepancy between uterine size and predicted AOG:fibroids,
incorrect menstrual dating, multiple gestation, and amniotic fluid anomalies
• The adnexa consists of the fallopian tube and the ovaries
Adnexa
• Palpate the adnexa & observe for masses and/or tenderness
• Evaluate the bony pelvic architecture
• Engagement: bi parietal diameter of the baby should enter the pelvic inlet
• Station: to determine how far the most dependent portion of the fetal
presenting part (cephalic or breech) is from the ischial spine:
Clinical
• Level of ischial spine: station zero "0"
pelvimetry
• Above the ischial spine, expressed with "minus" or"-" sign: -5 to -1
0 Below the ischial spine, expressed with "plus" or"+" sign: +l to +S

• Effacement: thinning out of the cervix

• Dilatation: progressive opening of the cervix (up to 10 cm)
• As required for complaints of rectal pain, bleeding or mass
Rectovaginal
• Allows for optimal palpation of the posterior cul-de-sac and uterosacral
examination
ligaments, as well as the uterus and adnexa

56
VII. PREGNANCYRISKASSESSMENT
• Purpose: identify pregnant women who are at an increased risk of maternal or fetal
morbidity and mortality

• Some conditions for which maternal-fetal medicine consultation may be beneficial include:
MEDICAL HISTORY
• Moderate to severe cardiac disorders
• Uncontrolled chronic hypertension
• Prior venous thromboembolism
• Renal insufficiency
• Severe restrictive or obstructive
pulmonary disease (e.g., severe asthma)
• Diabetes mellitus with end-organ damage
or uncontrolled hyperglycemia
• Family/personal history of genetic
abnormalities
• Hemoglobinopathy
• Autoimmune disorders or other severe
systemic disease
• Poorly controlled or complicated epilepsy
• Others: HIV infection, cancer, bariatric
surgery
Source:Cunningham,
I
I OBSTETRICAL HISTORY
• COE (Rh) or other blood group .
alloimmunization (excluding ABO, Lewis)
• Fetal structural or chromosomal
abnormality
• Desire or need for prenatal diagnosis or
fetal therapy
• Periconceptional exposure to teratogens
• Infection with or exposure to organisms
that cause congenital infection
• Higher-order multifetal gestation
• Amniotic fluid volume severe disorders
FG.WilliamsObstetrics25thEdition.2018

PRENATAL SURVEILLANCE
I. FETALSURVEILLANCE:
• Includes fetal heart rate, size (current & rate of change), amniotic fluid, presenting part
and station (late in pregnancy), and activity

• Used to monitor fetal growth and amnionic fluid volume

• Measured as the distance along abdominal wall from the top of symphysis pubis
Fundal
to the top of the fundus (bladder should be emptied prior measurement)
height
• Obesity or presence of uterine masses (e.g., myoma) may limit fundal
height accuracy
• Normal fetal heart rate: 110-160 bpm
Fetal heart
• Using Doppler ultrasound: FHT heard at 10-12 weeks
sounds
• Using stethoscope: FHT heard at 16 weeks (earliest)
• Provides information regarding fetal anatomy, growth and well-being
• Physician is not obligated to perform sonography without a specific
Sonography
indication in a low-risk patient, but that if patient requests sonographic
screening, it is reasonable to honor her request
Source:ACOG;2016

II. MATERNALSURVEILLANCE:
• Vital signs: blood pressure, weight
• Check for symptoms, including headache, altered vision, abdominal pain, nausea and
vomiting, bleeding, vaginal fluid leakage, dysuria
• Abdominal exam (e.g., fundal height)
• Vaginal exam (e.g., confirm presenting part & station, pelvic capacity, and cervical
consistency, effacement and dilatation)

57
DATING OF PREGNANCY
• Pregnancy begins with the fertilization of ovum (exact time is usually unknown)
• Accurate determination of gestational length is one of the most important functions of
prenatal care
• The mean duration of pregnancy calculated from the first day of the last normal
menstrual period is very close to 280 days or 40 weeks

Normal Pregnancy Duration

General Terms:
• Non-viable pregnancy is less than or equal to 20 weeks gestation (140 days)
• Viable pregnancy:
0Preterm: >20 weeks to <37 weeks (141 to <259 days)
0Term: 37 weeks to 42 weeks (259-294 days)
0Post term: >42 weeks (>294 days)
Term Pregnancy Categories
(ACOG/SMFM:'Term Pregnancy" is further classified into the following categories)
• Early term: 37 weeks to 38 weeks and 6 days
• Full term: 39 weeks to 40 weeks and 6 days
• Late term: 41 weeks to 41 weeks and 6 days
• Postterm: ~42 weeks
Pregnancy divided into Trimesters:
• First trimester is from conception to 14 weeks gestation
• Second trimester is from 14 1/7 weeks to 28 weeks completed gestation
• Third trimester from 28 1/7 weeks to 42 weeks gestation
Source:ACOG/SMFM

I. CLINICALDATING
A. Determining Age of Gestation (AOG) using the Last Normal Menstrual Period (LNMP)
Age of gestation or gestational age (AOGor GA),which is the approximate age of the
0

fetus, is measured from the LNMP

Developmental age (DA) or conceptional/embryonic age refers to the number of weeks
0

and days since fertilization

AOGis usually 2 weeks more than the DA
0

Example: Date Consulted: May 27 2021; EDC:June 28 2021; LNMP: September 21, 2020

Using LNMPto compute for AOG

LNMP: 09/21/20
0

Date Consulted: 05/27 /21

0

09/21/20 (LNMP)
9/ 21-30/20 (from Sept 21-30) = 10 days

September = 10 days
October = 31
November = 30
December = 31
January = 31
February = 28
March = 31
April = 30
May = 27 (from May 1,2021 up to time of consult)
249 days

249 days divided by 7 days = 36 weeks and 4 days--+ AOG during consult

58
B. Determining
0

0
Expected Date of Delivery (EDD) using LNMP
Most reliable clinical indicator of gestational age is an accurate LNMP
Average duration of pregnancy is 280 days from the first day of LNMP (40 weeks)
• It is apparent that pregnancy begins on the average 2 weeks before ovulation
N-_a--'eg"-e_l_e_R_u_l_e
_____________________________ .,
I
•
• Estimation of pregnancy due date: add 7 days to the first day of LNMPand subtract 3
months then add 1 year
• Example: first day ofLNMP is September 21, 2020 ----+ due date is June 28, 2021
• When using this, we assume that ovulation and conception on the 14th day of a 28 day cycle
Expected Date of Delivery (EDD)
• To the first day of the last normal menstruation, add seven days, subtract three months
and add one year
LNMP
0

, +7 to the day
, -3 months
+l year
0

Examples:
LNMP was June 29, 2020 LNMP was July 10, 2020 LNMP was January 1, 2021
(6/29/2020) (7/10/2020) (01/01/2021)

6 29 2020 7 10 2020 1 1 2021

-3 +7 +l -3 +7 +l -3 +7
4* 6 2021 4 17 2021 10 8 2021

EDD:April 6, 2021 EDD:April 17, 2021 EDC = October 8, 2021

'carryover1

C. Dating by Quickening (perception of movement of the fetus by the mother)

Quickening is the maternal perception of fetal movement can give a rough estimate of
0

duration of pregnancy
Used as a confirmation method rather than a primary method
0

Quickening or movement is usually perceived initially:

0

• For primigravidas: at 18-20 weeks AOG

• For multigravida: at 16-18 weeks AOG

59
 D. Height of the Fundus
0 Progressive enlargement of the uterus can be followed during pregnancy
0 Height of the fundus can be used to estimate the gestational age
GESTATIONAL AGE I HEIGHT OF THE FUNDUS
12 weeks after LNMP • Above the pubic symphysis
16 weeks after LNMP • Halfway between symphysis and the umbilicus
20 weeks after LNMP • Level of the umbilicus
36 weeks after LNMP • Below the ensiform cartilage (xiphoid process)

II. ULTRASOUNDDATING
• Most reliable method for establishing fetal dating especially when the mother is unsure of
menses or the mother has irregular menses
• Ultrasound dating is most accurate in the first 12 weeks of pregnancy (1st trimester)
• The earlier sonography is performed, the more accurate the gestational age assessment
• Sonographic gestational age should be used when the LNMP-derived gestational age
differs from that obtained with sonography by the threshold value

Guidelines for Reda ting Based on Ultrasonography*

GESTATIONAL AGE I PARAMETER($) I THRESHOLD TO REVISE
< 9 weeks >5 days
• Crown-rump length
9 to <14 weeks >7 days
14 to <16 weeks >7 days
• Biparietal diameter
16 to <22 weeks • Head circumference >10 days
22 to <28 weeks • Abdominal circumference >14 days
• Femur length
~28weeks >21 days
'LNMPdeterminestheAOG;but,ifultrasoundand LNMPdifferby the thresholdcut-off,ultrasoundis used fordating.

Examples:
• Example 1: based on LNMP,AOG is 9 weeks; but based on a CRL,AOG is only 7 117 weeks:
since the difference is >5 days between the LMP and ultrasound dating, we follow the
ultrasound dating
• Example 2: based on LNMP (mother is sure of last menses & has regular menstrual cycles),
AOG is 14 weeks and based on BPD via ultrasound, AOG is 13 5/ 7 weeks: we can still use 14
weeks because the difference between the two measurements is less than 7 days

Source:ACOG;2017

Crown-Rump Length (CRL}

• Most accurate: use the Crown-Rump Length (CRL) at 8-12 weeks
• When the embryo is evident, CRL s8+6 weeks of gestation is the most accurate biometric
parameter for pregnancy dating (±5 days)

• CRL is the longest straight-line

measurement of the embryo measured
from the outer margin of the cephalic pole
to the rump

60
NUTRITIONAL COUNSELING IN PREGNANCY
I. BASICTENETS FOR NUTRITIONPLAN

I
• Advise the pregnant woman to eat food types she wants in reasonable amounts and
salted to taste
• Ensure that food is amply available for socioeconomically deprived women
• Monitor weight gain, with a goal of ~25-35 lbs in women with a normal BMl
• Explore food intake by dietary recall periodically to discover the occasional nutritionally
.
errant diet

II. WEIGHTGAIN
• This table shows the body mass index (BMl) cut-off from the World Health Organization
(WHO), Institute of Medicine (!OM) and the American College of Obstetricians and
Gynecologists (ACOG)
• This table also shows the expected weight gain per week starting 2nd trimester, and the
total weight gain expected during the whole duration of pregnancy

Category
1•..(WHO)
.,,,.;,,. I {ACOG)
BMl I To<al
weight
I To<al
weight
I wo;gtrt ga;o ,.,
wee~
(kg/m 2 ) (kg/m 2 ) . (k ) . (lb ) (2nd-3rd trimester)
gain g gain s (lbs)

Underweight <18.5 <19.8 12.5 - 18 28 - 40 1 (1-1.3)

Normal 18.5 - 22.9 19.8- 26 11.5 - 16 25 - 35 1 (0.8-1.0)

Overweight ~23.0 26 - 29 7 - 11.5 15 - 25 0.6 (0.5-0. 7)

Obese ·-· >29 5 • 9.1 11-20 0.5 (0.4-0.6)
Source: Cunningham,FG. WilliamsObstetrics25th Edition.2018

Ill. NUTRITIONALREQUIREMENTS
A. Calories and Protein

• Caloric increase of 100 to 300 kcal/day is recommended during pregnancy

Calories • Second trimester: increase of 340 kcal/day
• Third trimester: increase of 452 kcal/day

• Protein requirements increase to meet the demands for growth and

remodeling of the fetus, placenta, uterus, and breasts, and for increased
maternal blood volume.
Protein
• During the second half of pregnancy, 1,000g of protein are deposited
• Recommendation: 1 g/kg/day
• Sources: meat, milk, eggs, cheese, poultry, fish
Source:MP, AGOG,2017
IOM,2006

B. Total Energy Requirement

Formula:
Total Energy Requirement (TER) = Desirable body weight (DBW) x Activity level

Computation of Desirable Body weight

DBW= Height ( cm) - 100

**For Filipinos: DBW - 10% of DBW

61
 Total Energy Intake for Gravida (kcal/kg/day)
ACTIVITY LEVEL I UNDERWEIGHT I NORMAL I OVERWEIGHT
Sedentary (mostly sitting) 35 30 25
Light (driver, nurse, MD) 40 35 30
Moderate (manual labor) 45 40 35
Very active (farming) --- 45 ---
Source:POGSCPGon MaternalNutrilion
& Supplementation,
2018

Example: Filipino, call center agent (sedentary), Normal BM/, Height =163 cm
DBW= height (cm) - 100 = 163 - 100 = 63 kg
Since patient is a Filipino: 63 kg- 6.3 (which is 10% of 63 kg)= 56.7 kg
TER = Desirable body weight (DBW) x Activity level
= 56.7 kg x 30 (activity level for a sedentary patient with normal BMI)
= 1,701 kcal
Since the patient is pregnant, add 100 to 300 kcal/day to TER
1,701 kcal (TER) + 300 kcaljd = 2,001 kcal/day

C. Macronutrient Distribution in Pregnancy and Lactation

ACTIVITY LEVEL I PROTEIN

(% OF ENERGY)
I TOTAL FAT
(%OF ENERGY)
I CARBOHYDRATE
(% OF ENERGY)

Pregnant:
TER + 300 kcal/kg/day
6-15 15-30 55-75
Lactating:
TER + 500 kcal/kg/day
Source:POGSCPGon MaternalNutrition
& Supplementation,
2018

IV. SUPPLEMENTATION
A. Minerals

MINERAL I DOSE
I REMARKS
• Calcium carbonate 500 mg • Target group: all pregnant women,
Calcium (elemental calcium) tablet, 3x a day particularly those at higher risk for
at 20 weeks AOG gestational hypertension
• 12 mg/day, but safe level for
• Deficiency: poor appetite, suboptimal
Zinc pregnant women not been clearly
growth, and impaired wound healing
established
• Use of iodized salt in preparing food
• 220 ug/day or 250 ug/day for • Sources: di/is, pusit, kuhol, lato, ta/aha,
Iodine
pregnant & lactating women tahong, alamang shrimps, crab
• Deficiency: cretinism, neurologic deficits
Source:DOHMemoNo.2016-0161Calciumsupplementation
for PregnantWomen
POGSCPGon MaternalNutrition& Supplementation,2018
RA8172:ASINLawof 1995

62
B. Iron Supplementation
, Give tablets of simple iron salts that provide at least 27 mg of elemental iron daily
, Recheck the hematocrit or hemoglobin concentration at 28 to 32 weeks' gestation to

I
detect significant anemia
INDICATION FOR DOSAGE
CATEGORY

Childbearing
I SUPPLEMENTS
I SCHEDULE I DURATION
.
• Anemia prevalence
• 3 months
age >40%
• Elemental iron: • As soon as possible
30-60 mg/day after gestation
• Universal
Pregnant • Folic acid: • Starts no later than 3rd
supplementation
400 mcg/day month and duration of
pregnancy
• Anemia prevalence
Lactating • 3 months postpartum
>40%

C. Folic Acid Supplementation (Vitamin B9)

, Deficiency may lead to megaloblastic anemia during pregnancy.
'Half of neural tube defects can be prevented with daily intake of 0.4 mg of folic acid
daily throughout the preconceptional period
, Sources: deep-green colored leafy vegetables, mustard & Philippine spinach, animal liver

GROUP I RECOMMENDATION

Women of • Folate rich foods

reproductive • Daily supplementation with 0.4 mg (400 mcg) folic acid
age • Counsel about folic acid supplementation to prevent birth defects
Women • A woman with a prior child with neural tube defect is considered high risk
high risk for
• Intake of 4 mg folic acid can reduce the 2-5% recurrence rate by 70%
having a baby
• Begin at least 30 days before pregnancy and to continue daily through
with neural
tube defect the first trimester

Source:POGSCPGon MaternalNutrition
& Supplementation,
2018

63
D. Other Vitamins

~
RATIONALE FOR RECOMMENDED
VITAMIN
I NUTRIENT INTAKE (RNI)

• Maintain adequacy in the well-nourished

Vitamin A
• High doses (>10,000 IU/day) is 750 750
(ug RE)
associated with congenital malformations
• Maintain a serum 25-0H vitamin D level
>20 ng/mL to prevent lione mass density
Vitamin D abnormalities
15 15
(ug) • Maternal deficiency: disordered skeletal
homeostasis, congenital rickets, and
fractures in the newborn
• Needed to protect lipids from
Vitamin E
peroxidation & permits normal 15 19
(mg a-TE)
physiological function
• Based on the 1 ug/kg body weight
Vitamin K (ug) 90 90
required for normal blood coagulation
Vitamin Bl • Amount required for normal erythrocyte
1.4 1.4
Thiamine (mg) transketolase activity
• Based on required level to maintain
normal erythrocyte glutathione reductase
VitaminB2 activity and urinary riboflavin levels.
1.4 1.6
Riboflavin (mg) • Deficiency may lead to angular stomatitis,
cheilosis, glossitis & seborrheic
dermatitis
• Amount required to achieve normal
Vitamin B3
levels of N-methyl nicotinamide urinary 18 17
Niacin (mg NE)
excretion

• Maintenance of normal hematologic

status and serum B6 levels
VitaminB6 • Deficiency may manifest as: insomnia,
1.9 2.0
Pyridoxine (mg) confusion, nervousness, depression,
irritability, peripheral neuropathy, motor
function impairment
• Maintain normal blood status as
measured by hemoglobin, MCVand
normal serum cobalamin levels
Vitamin B12 • Occurs naturally in foods of animal origin,
2,6 2.8
Cobalamin (ug) and strict vegetarians may give birth to
neonates whose B12 stores are low
• Deficiency, similar to folate, may elevate
the risk of neural-tube defects

• Maintain near-maximal neutrophil

VitaminC
concentration with minimal urinary 85 120
Ascorbic Acid (mg)
ascorbate excretion
RE - retinolequivalent
a-TE - alpha-tocopherolequivalent
NE- niacinequivalent
Source: Instituteof Medicine2006 and 2011

64
COMMON CONCERNS
• In the absence of complications, most women can continue to work until

I
the onset of labor
• With physically demanding work, women had 20-60% higher rates of
Employment
preterm birth, fetal-growth restriction, or gestational hypertension
• Advise women with prior pregnancy complications that commonly recur .
to minimize physical work
• Encouraged to engage in regular, moderate-intensity physical activity for
at least 150 minutes each week
• Safe activities: walking, running swimming, stationary cycling, and low-
impact aerobics
• Contraindications to exercise during pregnancy:
Exercise
, Significant cardiovascular or pulmonary disease
, Significant risk for preterm labor: cerclage, multiple gestation,
ruptured membranes
, Obstetrical complications: preeclampsia, placenta previa, fetal growth
restriction
• Pregnant and lactating women are advised to avoid specific types of fish
Seafood
with potentially high methylmercury levels like shark, swordfish, king
consumption
mackerel, and tile fish
Lead • Significant lead exposure is associated with gestational hypertension,
screening miscarriage, low birthweight, and neurodevelopmental impairments
• Properly positioned three-point restraints against automobile crash injury:
, Lap portion of the restraining belt is placed under the abdomen and
across her upper thighs
Automobile &
, Belt should be comfortably snug
air travel
, Shoulder belt is firmly positioned between the breasts
• Pregnant women can safely travel by air up to 36 weeks AOG,in the
absence of obstetrical and medical complications
• Sexual intercourse usually is not harmful, specifically late in pregnancy.
Coitus • Whenever miscarriage, placenta previa, or preterm labor threatens,
coitus is avoided
• Examination of the teeth is included in the prenatal examination, and
Dental care good dental hygiene is encouraged
• Periodontal disease has been linked to preterm labor
• Caffeine intake during pregnancy be limited to <300 mg/day, which
Caffeine
approximates three 5-oz cups of percolated coffee
• Two types of cord blood banks:
, Public: promote allogenic donation, for use by a relative or unrelated
Cord blood
recipient, similar to blood product donation
banking
, Private: store stem cells for future autologous use and charged fees for
initial processing and annual storage.
Source:Cunningham,
FG.WilliamsObstetrics25thEdition;2018
AmericanDieteticAssociation:2008
ACOG;2016and2017
Armson;2015

65
IMMUNIZATION FOR FILIPINO PREGNANT WOMEN
I. GENERALCONSIDERATIONS FORVACCINATION
• Never administer in the buttock.
• Confirm completion of childhood (or more recent) primary vaccine series for measles,
mumps, rubella (MMR) and Tetanus-Diphtheria (Td) before initiating recommended
vaccine schedules.
• Maintain vaccine administration record in patient's chart
Simultaneous use of any vaccines is not contraindicated
• Antibiotic therapy or breastfeeding are not contraindications to vaccination

II. SUMMARYOF VACCINES

FORALLFILIPINOWOMEN

;,10 years • HPV IM • 3 doses: 0, 1-2 months, and 6 months

• 3 doses: 0, 1, 6-12 months

• Tetanus-diptheria toxoid IM
• Booster: every 10 years
• 3 doses: 0, 1, 6 months
• Hepatitis B vaccine IM
• Booster not routinely recommended
18 to 50 • Measles, mumps, rubella* SC • 2 doses: 0, 1 month
years
• Varicella vaccine* SC • 2 doses: 0, 1 month

• 1 dose once every year from

• Influenza vaccine IM
February to June

• Hepatitis A IM • 2 doses: 0, 6-12 months

• Pneumococcal vaccine IM • 1 dose (revaccination after 5 years)

• 1 dose once every year from

• Influenza vaccine IM
February to June

;,50 years • 3 doses: 0, 1, 6-12 months

• Tetanus-diphtheria toxoid IM
• Booster: every 10 years

• 3 doses: 0, 1, 6 months
• Hepatitis B vaccine IM • Booster not routinely
recommended

Pregnant
• 3 doses: 0, 1, 6-12 months
0 1st dose: Td
• Tetanus-diptheria (Td)
toxoid
IM 0 2nd dose: Tdap

0 3rd dose: Td

• Booster: every 10 years

Any age • 1 dose once every year from
• Influenza vaccine IM
February to June

• 3 doses: 0, 1, 6 months
• Hepatitis B vaccine IM
• Booster not routinely recommended

• COVID-19vaccine•• IM • Follow recent guidelines

'Measles, mumps, rubella(MMR)and varicellavaccines are liveattenuated vaccines. Allthe others discussed
above are inactivatedvaccines.
.. At the timeof writing,COVID-19vaccine is also recommendedfor non-pregnantwomen. For pregnant women,
COVID-19vaccine is allowedin any trimester.Followthe most recent guidelines.
Source: POGS Task Force on Immunizationfor Women,2010

66
III. IMMUNIZATIONFORPREGNANTWOMEN
INDICATIONS
DURING
PREGNANCY I SCHEDULE
I REMARKS

Tetanus-Diphtheria (Td) and Tetanus-Diphtheria-Pertussis

• Pregnant women with
no previous tetanus
immunization or unknown
tetanus immunization history
should receive three doses of
Td vaccine
• Pregnant women whose last
Td/Tdap vaccination was
> 10 years ago should receive
Td booster in the 2nd or 3rd
trimester of pregnancy
Influenza Virus Immunization
• All pregnant (regardless of
trimester) and breastfeeding
women should receive the
inactivated flu vaccine
Hepatitis·B Virus (HBV)Immunization
• Indicated in pregnant women
who are eligible
• All HBsAg negative pregnant
women seeking ST! treatment
who have not been previously
vaccinated should receive
HBVvaccination
• Primary tetanus
immunization series
consists of three Td
injections given IM
(Tdap} Immunization
(deltoid)
• First two doses given one
month apart (starting
in 2nd trimester), and
third dose can be given
postpartum as Tdap
• Given one dose IM,
every year
• Given IM in 3 doses at
0, 1, 6-12 months
• Td vaccine is preferred
over Tetanus Toxoid
(TT) because of the
additional protection
I
.
against diphtheria
• Contraindicated if with
severe allergic reaction
after a previous dose
• Contraindicated if with
severe allergic reaction
after a previous dose
,.o
• Contraindications
include severe allergic
reaction to vaccine and
patients with moderate
to severe acute illness

IV.GENERALCONTRAINDICATIONS TO VACCINATION
• Severe allergy to vaccine components
• Pregnancy (or planning pregnancy within four-weeks) for live attenuated vaccines (e.g.,
measles, mumps, rubella, varicella)
• Severe immune attenuation (for live attenuated vaccines only)
• Moderate or severe acute illness
• If a live attenuated vaccine is given simultaneously with another vaccine, a four week
separation interval should be used between vaccinations.

67
 SECTION FOUR
ANTENATAL SURVEILLANCE
OVERVIEW OF ANTEPARTUM FETAL SURVEILLANCE
I. INDICATIONS
• Generally, these tests are used in pregnancies with a high risk of antepartum complications
• Some conditions include the following:
MATERNAL CONDITIONS I PREGNANCY-RELATED CONDITIONS
• Antiphospholipid antibody syndrome • Pregnancy-induced hypertension
(APAS), SLE • Decreased fetal movement
• Hyperthyroidism, poorly controlled • Amniotic fluid volume abnormalities ( e.g.,
• Severe cardiac disease ( e.g., cyanotic oligo/polyhydramnios)
heart disease, hypertension) • Intrauterine growth restriction
• Post-term pregnancy
• Prior fetal demise
• Multiple gestation with significant growth
discrepancy
Source:PrebothM.ACOGguidelines.AmFam Physician;2000

II. TECHNIQUESFORANTEPARTRUMFETALSURVEILLANCE
• Electronic fetal monitoring
0 Non-stress test (NST)
° Contraction stress test (CST)
• Ultrasound modalities
0 Umbilical artery Doppler velocimetry
0 Biophysical profile (BPP)

NON-STRESS TEST (NST)

• In this test, the heart rate of the fetus that is not acidotic or neurologically depressed will
temporarily accelerate with fetal moment
• This is a test of fetal wellbeing before the onset of labor, used from 32 weeks AOG to term
(diagnostic value before 32 weeks varies)
• Fetal heart rate acceleration in response to fetal movement (or fetal heart rate reactivity)
is an indicator or sign of fetal health and normal fetal autonomic function
• Loss of reactivity may be associated with CNSdepression, fetal acidosis, or a fetal sleep cycle

I.PROCEDURE
• NST measures the FHR in response to fetal movements
• An external FHR monitor is positioned and the mother (or an observer) is asked to push a
button (i.e., event marker) each time she feels fetal movement
• NST involves 20 minutes of monitoring the FHR while assessing accelerations that
correlate with fetal movement

Definition of Fetal Heart Rate (FHR)Acceleration (see Chapter 3 for details)

• Visually apparent abrupt increase ( onset to peak in less than 30 sec) in FHR
• At ;o,32weeks: acceleration >15 bpm from baseline, lasts for> 15 secs, but <2 mins from
onset to return
• At <32 weeks: acceleration ;o,10bpm from baseline, lasts for 10 secs, but <2 mins from
onset to return

68
II. INTERPRETATIONOF THE NON-STRESS TEST
0
INTERPRETATION DESCRIPTION*

I
• ;o,2accelerations peak at ;o,15bpm, each at ;o,15secs, and all
Reactive NST
occurring within 20 minutes**
Nonreactive NST • Lacks sufficient FHR accelerations over 40 minutes .
'Presence of fetal movementsand FHRaccelerationis the most criticalfeature of the NST
.. An abnormalstress test is not alwaysominousand can occurwitha sleepingfetus. Ifa test is not reactive,FHR
shouldbe monitoredfor at least 40 minutesto accountfor the fetus sleep cycle
Source: PrebothM.ACOGgu1dehnes.AmFam Phys1c1an; 2000

CONTRACTION STRESS TEST (CST)

• Based on the response of the fetal heart rate to uterine contractions
• It is believed that fetal oxygenation will be transiently worsened by uterine contractions
• Interpreted by the presence/absence of late FHR decelerations (i.e., decelerations that
reach their nadir after the peak of the contraction & persists beyond the and of the contraction)
• The CST is a test of uteroplacental function usually performed prior to induction of labor
• lfuteroplacental pathology is present, late decelerations would be apparent

I. PROCEDURE
• Fetal heart rate and uterine contractions are recorded simultaneously with an external monitor
• Contractions may be elicited using nipple stimulation or oxytocin infusion
Nipple stimulation: woman rubs her nipple through her clothing for 2 minutes or until
the contraction begins
Oxytocin: IV infusion is initiated at a rate of0.5 mU/min and doubled every 20 minutes
until a satisfactory CST result is established
• See definitions of FHR decelerations in Chapter 3

II. INTERPRETATIONOF THE CONTRACTIONSTRESS TEST

CST RESULT I INTERPRETATION
• No late or significant variable decelerations
Negative
• It is a normal finding (i.e., no uteroplacental insufficiency)
• Late decelerations following >50% contractions (even if there are
Positive <3 contractions in 10 min)
• It is an abnormal finding and may indicate uteroplacental insufficiency
Equivocal·
• Intermittent late or significant variable decelerations
suspicious
Equivocal- • Decelerations in the presence of contractions more frequent than
hyperstimulatory every 2 min or lasting longer than 90 sec
Unsatisfactory • <3 contractions in 10 min or uninterpretable tracing

UMBILICAL ARTERY DOPPLER VELOCIMETRY

• Doppler ultrasound is used to evaluate placental blood flow in cases of intrauterine
growth restriction
• Used to assess the hemodynamic components of vascular impedence
• Flow velocity waveforms in the umbilical artery of fetuses with normal growth differ from
those with growth restriction

I
UMBILICAL ARTERY FLOW
FETUS
VELOCITY WAVEFORM
Normally growing fetus • High-velocity diastolic flow
Intrauterine growth restriction • Diminished diastolic flow
Extreme intrauterine growth restriction • Absent or reversed flow

69
BIOPHYSICAL PROFILE (BPP)
• It is a combination of five fetal biophysical variables:
Fetal heart rate acceleration (NST)
Fetal breathing
Fetal movements
Fetal tone
0 Amniotic fluid volume (AFV)
• Normal variables are assigned a score of 2, and abnormal variables are assigned a score of 0

I. COMPONENTSAND SCOREFORTHE BIOPHYSICALPROFILE

COMPONENT I SCORE2
I SCORE0

Non-stress • 22 accelerations of 2 15 beats/min for • 0 or 1 acceleration within

test (NST}* 215 sec within 20-40 min 20-40 min
Fetal • 21 episode of rhythmic breathing lasting • <30 sec of breathing within
breathing ;,30 sec within 30 min 30min
Fetal • ;,3 discrete body or limb movements
• <3 discrete movements
movement within 40 min
• ;,1 episode of extremity extension and
Fetal tone • 0 extension/flexion events
subsequent return to flexion
• A pocket of amniotic fluid that measures
Amniotic fluid • Largest single vertical pocket
at least 2 cm in two planes perpendicular ,;2 cm
volume**
to each other (2 x 2 cm pocket)
BriefInterpretation:
• 8-10points:normal(exception:8/10withdecreasedAFVis consideredabnormal)
• 6 points:equivocal
• <4 points:abnormal
'May be omittedifallfoursonographiccomponentsare normal
*Furtherevaluation compositescore,if largestverticalamniotic
warranted,regardlessofbiophysical fluidpocket,;;2cm

II. INTERPRETATION
OF THE BPP
BPPSCORE I INTERPRETATION I RECOMMENDED MANAGEMENT
• No intervention
• Repeat test weekly except in diabetic
10 patients and postterm pregnancy
• Normal, non- (twice weekly)
NST not done (8/8)
asphyxiated fetus
• No intervention
But with normal AFV • Repeat testing per protocol
8 (8/10, AFVnormal}
But with low AFV • Suspected chronic
• Deliver
(8/10, AFV is zero) fetal asphyxia
• Deliver if:
• AFVabnormal
• Possible fetal • Normal AFV>36 weeks with
6 asphyxia favorable cervix
• Repeat test ,;6
• Repeattest >6:observe&repeat per protocol
• Probable fetal • Repeat testing on the same day
4 asphyxia • If BPP score :,6: deliver
• Almost certain
0-2 fetal asphyxia
• Deliver

'Note !hat8/10pointsis considerednormalifAFVis normal;and is consideredabnormalifAFVis decreased.

Source:Cunningham,FG.WilliamsObstetncs25thEd1t1on.
2018
ManningFA,el al.AmJ ObsletGynecol.1987
70
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2.American Academy of Pediatrics Committee on Fetus and Newborn and American College of Obstetricians and Gynecologists
Committee on Obstetric Practice. Guidelines for Perinatal Care, 8th, Kilpatrick SJ, Papile L (Eds), 2017.
3. AmeriarnAcademyof PediaOics,American CollegeofObstetridansand Gynero!ogists:
4. AmericanCollegeof Obstetriciansand Gynecologists:
Guidelinesforperinatalcare,8th ed.ElkGroveVillage,AAP,2017
Antepartumfetalsurveillance.PracticeBulletinNo.145,July2014, Reaffirmed2016
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;,
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: ,,
5. AmeriranCollegeofObstetridans and Gynecologists:Fetalgrowth restriction.PracticeBulletinNo.134,May2013,Reaffinned2015 ·_ •
6. AmericanCollegeofObsteOiciansand Gynecologists: Nauseaand vomitingof pregnancy.PracticeBulletinNo.153,September2015c
7. AmericanC.Ollegeof CommitteeOpinionNo700: Methodsfor Estimatingthe DueDate.ObsretGynerol2017; 129:e150.
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8.American Institute of Ultrasound in Medicine (AIUM):Official statements. Prudent use in pregnancy. 2012. Available at http://v ..rww.
aium.org/fficialStatements/33.
9.American Institute of Ultrasound in Medicine (AIUM):Practice guideline for the performance of fetal echocardiography. J Ultrasound
Med 32[61'\067, 2013a
10. Bertrand], Floyd LL,Weber MK;Fetal Alcohol Syndrome Prevention Team, Division of Birth Defects and Developmental Disabilities,
National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention (CDC).Guidelines for
identifying and referring persons with fetal alcohol syndrome [published correction appears in MMWRMorb Mortal Wkly Rep. 2006
May 26;55[20)568]. MMWR Recomm Rep. 2005;54(RR-11}:1-14.
11. Bilardo CM,WolfH, Stigter RH,et al: Relationship between monitoring parameters and perinatal outcome in
12. Callahan, Tamara L.(2013). Blueprints obstetrics &gynecology. Baltimore, MD :Lippincott Williams & Wilkins
13. Centers for Disease Control and Prevention: Guidelines for vaccinating pregnant women. 2016. Available at: http://www.cdc.gov/
vaccines/pubs/downloads/b_preg_guide.pdf. Accessed February 2, 2021
14. Centers for Disease Control and Prevention: Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid, and acellular
pertussis vaccine (Tdap) in pregnant women-Advisory Committee on Immunization Practices {ACIP),2012. MMWR62(7):131, 2013b
15. Clark SM, Dutta E, Hankins GD:The outpatient management and special considerations of nausea and vomiting in pregnancy. Semin
Perinatol 38(8):496, 2014
16. ClinicalPracticeGuidelineson DiabetesMellitusin PregnancyThird Edition 2018. PhilippineObstetricaland Gynecological
Societyfoundation, Inc.
17. Cunningham, F.G., Leveno, K J.,Bloom, S. L.,Spong. C. Y.,Dashe, J.S., Hoffman, B. L.,Sheffield,J.S. (2018). Williams obstetrics (25th
edition.). New York: McGraw-HillEducation.
18. Development workshop report on electronic fetal monitoring: update on definitions. interpretation, and research guidelines. Obstet
Gynecol 112:661, 2008
19. FirthHY,BoydPA.01amberlainP,etal: Severelimbabnomialitiesafter chorionvillussamplingat 56-66 days'gestation lancet 337(8744):762,1991
20. Freeman RK:The use of the oxytocin challenge test for antepartum clinical evaluation of uteroplacental respiratory function. Am J
ObstetGynecol 121:481, 1975
21. Hoyme HE, May PA,Kalberg WO,et al. A practical clinical approach to diagnosis of fetal alcohol spectrum disorders: clarification of the
1996 institute of medicine criteria. Pediatrics. 2005;115(1):39-47. doi:10.1542/peds.2004-0259
22. Hsieh FJ,Shyu MK,Sheu BC,et al: Limb defects after chorionic villus sampling. Obstet Gynecol 85( 1):84, 1995
23. Institute of Medicine and National Research Council: Weight Gain During Pregnancy: Reexamining the Guidelines. Washington, The
National Academic Press. 2009
24. Institute of Medicine: Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Washington, The National Academies
Press, 2006 [PubMed: N8K50960) [PubMed: 2388168]
25. Korevaar; T. I.,Steegers, E.A., de Rijke,Y.8., Schalekamp-Timmennans, S., Visser;W. E., Hofman, A..Jaddoe. V.W.,Tiemeier, H.,Visser;T.
J.,t..tedici,M.,& Peeters, R.P.(2015). Reference ranges and determinants of total hCGlevels during pregnancy: the Generation RStudy.
European journal of epidemiology, 30(9), 1057-1066. https://doi.org/10.1007 /s10654-015-0039-0
26. Lu, M. C.. & Lu, J.S. (2008). Prenatal Care. Encyclopedia of Infant and Early Childhood Development, 591-604. doi:10.1016/b978-
012370877-9.00127-4
27. Macones GA,Hankins GD,Spong CY,et al: The 2008 National Institute of Child Health and Human
28. Manning FA,Morrison I, Lange IR, Hannan CR,Chamberlain PF. Fetal biophysical profile scoring: selective use of the nonstress test.
Am J Obstet Gynecol. 1987;156(3),709-712. dod0.1016/0002-9378(87)90083-4
29. ManningFA.PlattW,SiposL:Anteparturnfetalevaluation:developmentofafetalbiophysicalprofile.Am J ObstetGyneml136:787,1980
30. Matthews A, Haas DM,O'Mathuna DP,et al: Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev
Mar 3:CD007575, 2014
31. NijhuisJG, Prechtl HF,Martin CBJr;et al: Are there behavioural states in the human fetus? Early Hum Dev 6:177, 1982
32. OepkesD,SeawardPG,VandenbusscheFP,etal: Dopplerultrasonographyversusamniocentesisto predict fetalanemia N EnglI Med355:156,2006
33. Philippine Clinical Practice Guidelines on the Diagnosis and Management of Urinary Tract Infections in Adults 2015 Update
34. Philippine Obstetrical and GynecologicalSocietyClinicalPractice Guidelineon Diabetes Mellitus in Pregnancy November2018
35. Preboth M. ACOGguidelines on antepartum fetal surveillance. American College of Obstetricians and Gynecologists. Am Fam
Physician. 2000 Sep 01;62[5),1184, 1187-8
36. SadovskyE,EvronS,WeinsteinD:Dailyfetalmovement recording in nonnal pregnancy.RivObstetGinecolPracticaMed Perinatal59:395, 1979a
37. Severe, early intrauterine growth restriction. Ultrasound Obstet Gynecol 23:199, 2004
38. Stillennan KP,Mattison DR. Giudice LC,Woodruff TJ. Environmental exposures and adverse pregnancy outcomes: a review of the
science. Reprod Sci. 2008;15(7):631-650. doi:10.1177 /1933719108322436
39. Sumpaico,W, Ocampo-Andres, I., Blanco-Capito LR.de las Alas-Camero, S. Diamante An, Gamilla ZN. (2008). Textbook of Obstetrics
3rd edition. Chapter 15 Diagnosis of Pregnancy
40. Todros T.Sciarrone A, Piccoli E,et al: Umbilical Doppler waveforms and placental villous angiogenesis in pregnancies complicated by
fetal growth restriction. Obstet Gynecol 93:499, 1999

71
LABOR
ANDDELIVERY
 SECTION ONE
MECHANISMS OF LABOR

INTRODUCTION TO MUST-KNOW CONCEPTS

■
I. DEFINITIONS OF TERMS
TERM I DEFINITION -
Nulligravida • Woman who has never been pregnant
Prirnigravida • Woman who is pregnant for the first time
Multigravida • Woman who has had more than one pregnancy
• Woman whose pregnancy never reached the age of viability
Nullipara (nulliparous)
(2'20 weeks)
• Woman who delivered only one fetus beyond the age of
Prirnipara (prirniparous)
viability (2'20 weeks)
Multipara (rnultiparous) • Woman who delivered ;,2 fetuses beyond age of viability

II. STATION
• Station is the extent to which the most dependent portion of the presenting part has
descended into the pelvis
• Descent of the leading edge of the presenting part to the level ofischial spines (station 0)
is defined as engagement
• Station +S means the fetal head/skull is 5 cm below the ischial spine, in which the fetal
scalp is almost separating the labia (make sure it is not the caput that is presenting)

-5
-4
-3
-2

lschial spine

+2 -·-·-·-·-·-·-·-
+3 -·-·-·-·-·-•-·-
+4 -·-·-----·---·-
+5 -·-·-·---------

Station -5 to +5, with the ischial spines as Station 0

• Stations are measured in centimeters (cm) above or below station 0

0Negative number: presenting part is above the level of the ischial spines
0Positive number: presenting part descends further into the pelvis
• In the descent pattern of normal labor, a hyperbolic curve is formed when the station of
the fetal head is plotted as a function of labor duration
• In nulliparas: descent is slow and steady
• In multiparas: descent may be rapid
75
III. THE FETAL HEAD
• The head is the largest and least compressible part of the fetus, which makes it the most
important part from an obstetric point of view

Anteriorfontanelle
Posterior (bregma)
fontanelle
Biparietal
diameter Glabella

Sagittal Posterior
Nasion fontanelle
suture

Anterior Bitemporal
fontanelle diameter
(bregma)

Occipitomental
diameter
Frontalsuture

Landmarks (from front to back):

• Nasion: root of the nose
• Glabella: elevated area between the orbital ridges
• Sinciput (brow): area between the anterior fontanelle and glabella
• Anterior fontanelle (bregma): diamond-shaped fontanelle
• Vertex: area between fontanelles and bounded laterally by the parietal eminences
• Posterior fontanelle (lambda): Y-or T-shaped fontanelle
• Occiput: area behind and inferior to the posterior fontanelle and lambdoid sutures

A. Sutures (membrane-occupied spaces between the cranial bones)

SUTURE
I DESCRIPTION

• Lies between the parietal bones

Sagittal suture • Extends in an anteroposterior direction between the fontanelles
Divides the head into right & left sides
Lambdoid • Extends from the posterior fontanelle laterally
suture • Separates the occipital from the parietal bones
• Extends from the anterior fontanelle laterally
Coronal suture
• Separates the parietal and frontal bones
• Lies between the frontal bones
Frontal suture • Extends from the anterior fontanelle to the glabella
(prominence between the eyebrows)

B. Fontanelles (spaces where sutures intersect)

FONTANELLE I DESCRIPTION

• Also known as "bregma"

Anterior
• Found at the intersection of the sagittal, frontal, and coronal sutures
fontanelle
• Diamond shaped and larger than the posterior fontanelle
Posterior • Triangle-, Y-or T-shaped
fontanelle • Found at the junction of the sagittal and lambdoid sutures

76
 C. Diameters

DIAMETER
I LENGTH
AVERAGE
FOR
I DESCRIPTION
TERM FETUS
Anteroposterior (AP) Diameters*
• Presenting AP diameter during flexion,

·Suboccipitobregmatic
Occipitofrontal
Supraoccipitomental
Submentobregmatic
Transverse Dit:,meters
Bi parietal
Bi temporal
'The APdiameterpresentingto the maternalpelvisdependson the degree of flexionor extensionof the head. It
is importantbecause these diametershave varyinglengths
■
when the chin is in intimate contact with
.
• 9.5 cm the thorax
• Extends from occipital bone to the
anterior fontanelle
• Presenting AP diameter in a sinciput
presentation during initial descent
• 11 cm
• Extends from external occipital
protuberance to the glabella
• Presenting AP diameter in brow
presentation
• 13.5 cm
• Longest AP diameter of the head
• Extends from the vertex to the chin
• Presenting AP diameter in face
presentations
• 9.5 cm
• Extends from neck/lower jaw to the
anterior fontanelle
• 9.5 cm • Largest transverse diameter
• Extends between parietal bones
• 8 cm • Shortest transverse diameter
• Extends between temporal bones

IV.THE FACTORSFORSUCCESSFULLABOR(3 P's)

• In normal labor, uterine contractions cause progressive dilation & effacement of the
cervix along with descent & expulsion of the fetus
• Normal labor progresses in a slower manner among nulliparous women
• Has to adapt itself through the birth canal
• Describes the fetal lie, attitude, presentation, and position which are
considered to be crucial
Passenger 0
Fetal lie: relation of the fetal long axis to that of the mother
(the fetus) 0
Fetal attitude: posture or habitus of the fetus
0 Fetal presentation: portion of the body that is foremost within
the birth canal
0
Fetal position: orientation of the presenting part to birth canal
Passage • A straight cylinder consisting of the pelvis where the fetus would
(birth canal) journey from the womb to the outside world
• Refers to the uterine contraction during the first stage of labor and
Power the uterine contraction and intra-abdominal pressure during the
second stage of labor

77
THE PASSENGER
• Orientation of the fetus within the uterus and in relation to the pelvic canal are essential
to a successful vaginal delivery
• Determining the correct fetal lie, presentation, attitude and position would aid in the
management of labor & delivery

1. Leopold Maneuvers (LM): discussed in detail in previous chapter

• LMl: to assess which fetal pole occupies the fund us
• LM2: to assess the fetal orientation
• LM3: to confirm the fetal presentation
• LM4: to determine degree of descent
2. Vaginal Examination
• Insert two fingers into the vagina to determine the presenting part
• If vertex is presenting, direct the fingers posteriorly and sweep forward toward the
maternal symphysis to determine linear course of the sagittal suture
• Ascertain the position of the two fontanelles, found at either end of the suture
Anterior fontanelle: large, diamond shaped
0

Occipital fontanelle: triangle shaped

0

• Establish the station or extent to which the presenting part has descended into the pelvis

I. FETALLIE
• Relation of the long axis of the fetus to that of the mother
• It may be longitudinal, transverse, or oblique

• Most common fetal lie

• Long axis of the fetus parallels the
Longitudinal
longitudinal axis of the uterus
lie (99%)
• Fetus lie on the same plane/line with the
long axis

• Fetus lies in the transverse or one of the

oblique diameters of the uterus
• Shoulder is usually over the pelvic inlet
with the fetal head lying in one iliac fossa
and the breech in the other
Transverse lie
• Another variant is the fetal back occupies
the fundus while the fetal small parts are
on the lower segment
• Predisposing factors: multi parity, placenta
previa, hydramnios, uterine anomalies

• Transient and unstable

Oblique lie • Becomes longitudinal or transverse lie
during the course of labor

Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018

78
II. FETALPRESENTATION(PRESENTINGPART)
• Portion of the fetal body that is either foremost within the birth canal or closest to it (i.e.,
part that lies closest to the pelvis and will enter the birth canal first)
• Felt through the cervix during internal examination
• May be cephalic, breech, shoulder, or compound presentation

A. Cephalic Presentation {most common presentation)

0The usual presenting part is the head (i.e., cephalic presentation) ■
0Most common presentation is the vertex (occiput) presentation (usually left occiput ~•·
transverse in 40%) · ·
0In cephalic presentation, we can feel the head in the cervix during internal examination •
0The head is thrust into the inlet and the lower segment of the uterus, resulting in
flexion of the f.lltalhead

TYPESOF
CEPHALIC
I DESCRIPTION
I PRESENTING
AP
I DIAGRAM
PRESENTATION DIAMETER*

• Head sharply flexed-

chin in contact with the --
Vertex or thorax
Occiput
Presentation
• Occipital fontanel is the • Suboccipito- ~ "\:£
(Most presenting part (we can bregmatic s
Common) readily feel the occipital - -- - _,.:__ -
fontanel - triangle ~/

shaped)

• Head only partially flexed

• Anterior fontanel or
Sinciput bregma (large, diamond
Presentation shaped) is the presenting • Occipito-
(Military part frontal
Attitude) • Usually becomes a vertex
presentation as labor
progresses

Brow
Presentation**
• Fetal head is only
partially extended
• Usually becomes a face
presentation as labor
• Occipito-
mental
(longest)
- -~-----
-
,
-
progresses - '. _P - , -
'.

• Fetal neck is sharply

extended
• We feel the fetal face in
• Submento-
the surface
Face bregmatic or
• Occiput comes in contact
Presentation** tracheo-
with the back
bregmatic
• Vaginal delivery may
result in injury to the
cervical spinal cord
'Anteroposterior(AP)diameters:whenthe fetusentersthe pelvis,the fetalheadis alongthe obliquediameters
ofthe pelvis(presenting
diameterdependson the presentingpart).Cephalicpresentation withthe narrowest
diameters(e.g.,vertex/occiput)
has the best potentialforvaginaldelivery
"Deflectionattitudes(browand face):factorsthatfavorextensionor preventheadflexionincludeneckmasses,
cordcoils,anencephaly, contractedpelvis,largebabies,or pendulousabdomen.Aslaborprogresses,sinciput
& browpresentations usuallyconvertintovertexor facepresentations
byneckflexionor extension,respectively
(failureto do so can leadto dystocia)
Source:Cunningham FG,et al. Williams
Obstetncs25thEd;2018
79
B. Breech Presentation
0 Buttocks (and/or foot) can be palpated in the cervix on internal examination (i.e., large
nodular mass is felt toward the pelvis)
0 Incidence much greater earlier in pregnancy
° Fetus positions itself to make use of the roomier fundus (head is not in the lower uterine
segment)
0 Stargazing fetus: term breech fetus with extremely hyperextended neck

TYPESOF
BREECH
PRESENTATION
I REMARKS I DIAGRAM

• Most common type of breech

presentation
• Thighs are flexed
Frank Breech
• Legs are extended over the
Presentation
anterior surface of the baby
(the feet lie in proximity to the
head)

• Thighs are flexed over the

abdomen
Complete Breech
• Legs flexed upon thighs
Presentation
• Feet present at the level of the
buttocks

• Incomplete breech with one

or both feet is/are below the
Incomplete or breech
Footling Breech • Single footling: one leg is
Presentation extended towards birth canal
• Double footling: both legs are
extended towards birth canal

Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018

C. Other Presentations
Shoulder Presentation I Compound Presentation

• Acromion processes palpated in the cervix
• Shoulder/acromion is usually presenting
into pelvic inlet in transverse lie
• Fetal back location (back down, back up)
helps determine type of uterine incision
during CS
• Fetal hand or foot prolapses alongside
the presenting vertex or breech
• Combination of hand with vertex or
breech: tends to resolve spontaneously
• Combination of foot and fetal head:
complicated by cord prolapse

80
III. FETALATTITUDE (POSTURE OF THE HABITUS)
• Characteristic posture in the later months of pregnancy
• It is the relation of the fetal parts to one another
, Fetus forms an ovoid mass that corresponds roughly to the shape of the uterine cavity

How does the Fetus Position itself Inside?

•
•
•
•
•
•
•
Ovoid mass
Folded or bent upon itself
Back markedly convex
Head is sharply flexed
Chin in close contact to chest
Thighs flexed over abdomen
Legs bent at the knees
..
lMII

• Arches of the feet rest upon anterior

surface of legs
Arms crossed over the thorax or
parallel to sides
• Umbilical cord lies in the space
between extremities

IV.FETALPOSITION
• Refers to the relationship ofan arbitrary point of the presenting part to the left or right
side of the maternal birth canal
• Steps in determining fetal position:

STEP I QUESTION
I ANSWER
• For vertex (occiput) presentation: occiput or posterior
fontanelle (soft triangular depression)*
• What is the
1 arbitrary point?
• For face presentation: fetal chin (mentum)
• For breech presentation: sacrum
• For shoulder: acromion (scapula)
• What is the • Right (arbitrary point towards the right)
2 position of the • Left (arbitrary point towards the left)
arbitrary point? • Transverse (arbitrary point located in the horizontal plane)
• What is the • Anterior (arbitrary point towards the symphysis pubis)
3 direction of the • Posterior (arbitrary point towards the sacrum)
arbitrary point? • Transverse (arbitrary point located in the horizontal plane)

'2/3 of the vertex(occiput)presentationare in the leftocciputposition(e.g., the occipitalforamenor the soft triangu-
Jardepressionis on the leftside). Otherexamplesfor the vertexpresentationare:
Leftocciputanterior(leftside, towardsthe abdomen)
Rightocciputtransverse(rightside, towardsthe middle)
Rightocciputposterior(rightside, towardsthe sacrum)

81
General Cance ts in Determinin Fetal Position

posterior
__
'0 _
, ~--. ____ -Left occiput
posterior

Right occiput
transverse
RIGHT LEFT

~
Left occiput
transverse

Right occiput Left occiput

anterior ANTERIOR anterior

SACRUM
OP

ROP LOP

ROT LOT

OA
PUBIC SYMPHYSIS

How to Determine Fetal Position:

0Divide the birth canal into 4 quadrants, as follows: anterio1; posterim; transverse,
maternal right side and maternal left side (see legend below)
0 Determine the location of the arbitrary point for the given presenting part. In the
diagrams above, the arbitrary point is the occiput (most common)

Possible Positions
0 LOA: left occiput anterior
0 LOT: left occiput transverse
0 LOP: left occiput posterior
0 OP: occiput posterior
0 ROP: right occiput posterior
0 ROT: right occiput transverse
0 ROA: right occiput anterior
0 OA: occiput anterior

82
SOME EXAMPLES
Example 1: LEFT OCCIPUT ANTERIOR (LOA} POSITION
Pubic symphysis

I LM 1 LM 2

R L -
mg

Occiput
Sacrum

• Fetal lie: longitudinal lie

• Fetal presentation: cephalic presentation, specifically vertex or occiput (this is because the
occipital fontanel is the presenting part)
• Fetal position: left occiput anterior (because the occiput is directed towards the left &
anterior side)

MANEUVER I FINDINGS
• The breech occupies the fund us which gives the sensation of a large,
LM 1 nodular mass
• The fetal back is felt as a hard, resistant structure on the left side of the
abdomen of the mother. The fetal back is directed anteriorly
LMZ • The fetal parts is felt as numerous small, nodular, mobile parts on the
right side of the abdomen of the mother
• The thumb and fingers of one hand grasp the lower portion of the
LM maternal abdomen just above the symphysis pubis
LM3 • The fetal head feels hard, round and more mobile. An unengaged fetal
head is easily dislodged and mobile on palpation
• The fetal back is felt on the left side of the abdomen while the cephalic
prominence is felt on the right side of the abdomen which describes a
LM4 normal fetal attitude
• Hands diverge if the head is engaged, while the hands converge if head is
not engaged
Internal • Posterior fontanelle (or occiput) occupies the left anterior quadrant (i.e.,
examination LOA)
• FHT heard over fetal back (in this case, the maternal left, since the fetal
Others
back is on the left side of the mother) and slightly below the umbilicus
Source:Cunningham
FG,et al. Williams
Obstetrics25thEd;2018

83
Example 2: LEFT SACROANTERIOR {LSA) POSITION

Pubic symphysis

l Fetal sacrum

Maternal sacrum

• Fetal lie: longitudinal

• Fetal presentation: breech (specifically, complete breech, because the thighs and legs
are flexed}
• Fetal position: left sacro-anterior (because the buttocks face anteriorly and towards the left}

MANEUVER I FINDINGS
LM 1 • Fundus is occupied by the head

• Fetal back is oriented anteriorly and occupies the left side of the
maternal abdomen.
LM2 • Fetal heart tones heard over fetal back Hence, it is best heard on the left
LM side of the maternal abdomen near the umbilicus
• If not engaged, movable breech occupying the lower pole above the
LM3 symphysis
LM4 • If engaged, breech beneath the symphysis

Internal • Fetal buttocks can be palpated (in addition, meconium staining of the
examination examining finger may occur)
• Fetal heart tones heard over fetal back (in this case, the maternal left}
Others
and slightly above the umbilicus
Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018

84
Example 3: LEFT MENTOPOSTERIOR(LMP)

Pubic symphysis

■
.

Sacrum Mentum

• Fetal lie: longitudinal

• Fetal presentation: face (specifically mentum posterior because the chin is facing the left
side of the maternal buttocks)
• Fetal position: left mentoposterior position

MANEUVER
I FINDINGS

LM1 • Fundus is occupied by the breech

• Fetal back is oriented anteriorly and occupies the right side of the
maternal abdomen
LMZ • Fetal heart tones heard over fetal back. Hence, it is best heard on the
right side of the maternal abdomen near the umbilicus
• The fetal head feels hard, round and more mobile
LM3 • An unengaged fetal head is easily dislodged and mobile on palpation
LM
• Helps identify the degree of descent and fetal attitude by facing the
mother's feet and the fingertips of both hands are positioned on either
side of patient's lower abdomen moving downwards to palpate the
LM4 presenting part
• The fetal back and the cephalic prominence is felt on the right side of the
abdomen which indicates an abnormal fetal attitude or a hyperextended
fetal head which indicates a face presentation
Internal • Fetal face palpated as irregular and soft
examination
• Fetal heart tones heard over fetal back (in this case, the maternal right)
Others
and slightly below the umbilicus

Source:CunninghamFG, et al. WilliamsObstetrics25th Ed; 2018

85
Example 4: LEFT OCCJPUT TRANSVERSE (LOT}

Occiput

• Fetal lie: longitudinal lie

• Fetal presentation: cephalic presentation, specifically vertex or occiput (this is because the
occipital fontanelle is the presenting part)
• Fetal position: left occiput transverse (because the occiput is directed towards the left side
in the horizontal plane)

MANEUVER I FINDINGS
• The fundus is occupied by the breech (buttocks/feet are in the fund us)
LM 1 • The breech is a large nodular mass
• The plane of the fetal back is on the mother's left side
LMZ • Fetal extremities (small, nodular, mobile parts) are located on the
maternal right side
LM • If the head is engaged, presenting part is not moveable (biparietal
LM3 diameter is through the pelvic inlet already)
• If head is not engaged, fetal head is easily dislodged on deep palpation
• Hands converge if head is not engaged
LM4 • Cephalic prominence on the right
• Fetal back is on the left
Internal • The sagittal suture occupies the transverse diameter of the pelvis
examination • The posterior fontanelle (triangular shaped) is on the left of the mother
• Fetal heart tone heard on the left side of the maternal abdomen at the
Others
level of the umbilicus
Source:Cunningham
FG,et al. Williams
Obstetrics25thEd;2018

86
THE PASSAGES (THE FEMALE BONY PELVIS)
• The pelvis is divided into the false pelvis (oflittle obstetric significance) and the true
pelvis (major portion of the birth canal)
• The descent of the fetus through the pelvis occurs through three important planes:
0Pelvic Inlet: the superior strait
0Midpelvis: plane of least pelvic dimensions
0Pelvic Outlet: the inferior strait

1
rll_lu_s_t_r_a
tiio~nio;,J;t;h;e;T;riu
e_P_e_lv_i_s
1 _______________________ 7 ■

PELVIS

I. PELVICINLET (SUPERIOR STRAIT)

l
• This is where the presenting part enters into the true pelvis
• Forms the brim of the true pelvis and shares the same anatomic borders
• The fetal head enters the pelvic inlet in the transverse position

CONJUGATES
Sacral
True conjugate A
Obstetrical conjugate B
Diagonal conjugate C

Anteroposterior

Pubic
symphysis

The inlet of the pelvis comprises of the pelvic brim, pubic bone, and sacral promontory
• Posterior border: sacral promontory and alae of sacrum
• Lateral border: linea terminalis
• Anterior border: horizontal pubic rami and symphysis pubis

The pelvic inlet has important diameters, illustrated above

• Anteroposterior diameter (see subsequent table)
• Transverse diameter: widest distance between iliopectineal lines (therefore, fetal head
wants to descend through this portion of the pelvis in an occiput transverse to align the
widest diameter of the head to the inlet)
• Each oblique diameter (right and left) extends from the sacroiliac joint to the opposite
iliopectineal eminence
87
Anteroposterior Diameters*
DIAMETER I MEASUREMENT I REMARKS
• Sacral promontory to lower margin of
symphysis pubis
Diagonal conjugate
• >11.S cm • Only the diagonal conjugate can be
(DC)
measured clinically:
• To measure the DC,see image below
• Shortest distance between the sacral
promontory and symphysis pubis
Obstetric conjugate • >10 cm
• Derived by subtracting 1.5-2 cm from the
diagonal conjugate
True/anatomic • Sacral promontory to upper margin of
• 11 cm
conjugate symphysis pubis
'Thistablespecifically
refersto anteroposteriordiameters
(oneofthefourdiametersofthe pelvicinlet).OnlyAP
diameteris showninthe table(notdiscussedhereare the transversediameterand obliquediameters).Thepelvic
diametersneedto be adequateforthe fetalheadto be ableto descendandvaginaldeliveryto occursuccessfully.
A
contractedpelvicinletusuallycausesdystocia,prematureruptureofmembranes,and fetalmalpresentation.

Measuring the Diagonal Conjugate

Diagonal
conjugate
• Diameters can be evaluated clinically to screen for pelvic inadequacy
• Pelvic inlet can be evaluated for its AP diameter: diagonal conjugate is measured from the
lower border of the pubis to the sacral promontory using the tip of the 2nd finger and the
point where the base of the index finger meets the pubis symphysis (see image above)
• The obstetric conjugate is estimated by subtracting 1.5-2 cm from the diagonal conjugate
• If the diagonal conjugate is c:l 1.5 cm, the AP diameter of the inlet is considered adequate

88
II. MJDPELVIS(MIDPLANE OR PLANE OF LEAST PELVICDIMENSIONS)
• Extends from the lower margin of the symphysis pubis through the level of the ischial
spines to the tip of the sacrum
• Measured at the level of the ischial spines
• A contracted midpelvis can cause transverse arrest of the fetal head

True conjugate A
Obstetrical conjugate

Diagonal conjugate
B

C
I
.

Anteroposterior diameter
of midpelvis

Sacral

Transverse of inlet E
lnterspinous diameter F
Obstetrical conjugate G

lschial spines
Pubic symphysis
Important Diameters in the Midpelvis:
• Anteroposterior (AP) diameter (2:ll.S cm): extends from the lower border of the pubis to the
sacral vertebrae (S4-SS junction)
• lnterspinous (transverse) diameter (2:10 cm): between the ischial spines

Clinical findings in midpelvis contraction

• lschial spines are prominent
• Pelvic sidewalls are convergent
• Sacrosciatic notch is narrow
Source:Cunningham
FG,et al.WilliamsObstetrics
25thEd;2018

89
Ill. PELVIC OUTLET (INFERIOR STRAIT)
• Consist of two triangular planes sharing a common base formed by a line joining the two
ischial tuberosities
• The anterior triangle is formed by the pubic arch (pubic angle: 90-100 degrees)
• The posterior triangle has the tip of the sacrum as the apex and the sacrotuberous
ligaments and ischial tuberosities as the sides

Pubic symphysis

Anterior triangle A

Posterior triangle B

Bituberous diameter C

Anteroposterior diameter
Anterior sagittal diameter
Posterior sagittal diameter

Important diameters of the Pelvic Outlet:

• AP diameter (11.5 cm): from the inferior edge of pubic symphysis to the tip of the sacrum
(widest diameter of the outlet, therefore the fetal head wants to rotate to an occiput anterior
position to move underneath the pubic arch and descend through the outlet)
• Bituberous (transverse) diameter (10 cm): distance between the ischial tuberosities

90
 SECTION TWO
PHYSIOLOGY OF LABOR
PREPARATION FOR LABOR
Physiologic Preparatory Events Before Actual Labor
EVENT I DESCRIPTION
• Fetal head settles into the pelvic brim, noted by the mother as a flattening
of upper abdomen & increased prominence of the lower abdomen
Lightening • Occurs ~2 or more weeks before labor in primigravids (usually at ~36
weeks AOG)
• Occurs until early labor in multigravids
• Irregular (usually painless) contractions of the uterus during the last 4-8
Braxton
weeks of pregnancy
Hicks
• Appear sporadically and are unpredictable
contractions
• Not associated with progressive cervical dilatation and effacement
• Before parturition, cervix becomes softer due to increased water content
and collagen lysis
Cervical • Effacement (or obliteration of the cervical canal) occurs as it is pulled-up
effacement and taken up into the lower uterine segment
• Onset of labor may be heralded by the passage of a small amount of
blood-tinged mucus from the vagina (i.e., "the bloody show")

PHASES OF PARTURITION OR LABOR

Initiation of Onset of Delivery of Restoration of

Conception parturition labor conceptus fertility

Phase 1 Phase 2 Phase 3 Phase 4

Quiescence Activation Stimulation Involution

Prelude to parturition Preparationfor labor Processesof labor Parturient recovery

Contractile unresponsiveness, Uterine preparedness for Uterine contraction, Uterine involution,

cervical softening labor, cervical ripening cervical dilation, fetal cervical repair,
and placental expulsion breastfeeding
(three stages of labor)

• Parturition can be divided into four overlapping phases that correspond to major
physiological transitions. These four phases should not be confused with the clinical
stages of labor (i.e., first, second, and third stages), which make up phase 3 of parturition

Source:Cunningham
FG,et al. WilliamsObstetrics
25thEd;2018

91
I. PHASE 1: UTERINE QUIESCENCE& CERVICALSOFTENING (comprises 95% of pregnancy]
A. Anatomic Changes during Phase I
CHANGES 1- REMARKS

• Undergo phenotypic modification to a noncontractile state, and uterine

muscle is rendered unresponsive to natural stimuli
• Uterine quiescence is achieved in part by:
Myometrium ODiminished intracellular crosstalk & reduced intracellular Ca2 • levels
0Progesterone lowers expression of contraction-associated proteins.
° Caspase 3 (anti-contractile agent) activation
0Uterotonin degradation
• Greater tissue compliance, yet remains firm and unyielding
• Maintenance of cervical anatomical and structural integrity is essential
for pregnancy to continue to term
Cervix
(softening) • Softening results from:
• Increased vascularity
° Cellular hypertrophy & hyperplasia
• Structural changes in the extracellular matrix

B. Functions of the Cervix during Pregnancy:

0 Maintenance of barrier function to protect the reproductive tract from infection
0 Maintenance of cervical competence despite increasing gravitational forces
• Extracellular matrix changes that allow progressive increases in tissue compliance

C. Braxton Hicks Contractions or False Labor

0Low-intensity myometrial contractions that do not cause cervical dilations
0Become more common toward the end of pregnancy especially in multi paras

II. PHASE2: UTERINEAWAKENINGOR ACTIVATION

• To prepare for labor, the myometrial tranquility of phase 1 must be suspended
• In this phase, there is a progression of uterine changes during the last few weeks of pregnancy
CHANGES I REMARKS

• Expression of contraction-associated proteins (CAP) increases uterine

irritability and responsiveness to uterotonins
Myometrial
• Formation of lower uterine segment from the isthmus: "lightening" occurs
changes
which is felt as "the baby dropped"
• Greater expression of oxytocin receptors in fundal myometrial cells
• Cervix undergo extensive remodeling: results in cervical yielding and
dilatation upon initiation of forceful uterine contractions
Cervical
• Changes noted in the following:
ripening
• Endocervical glands occupy most of the cervix
• Dispersion of collagen fibrils:·loss of tissue integrity & increased compliance

III. PHASE 3: UTERINESTIMULATIONOR ACTIVELABOR

• Characterized by regular uterine contractions, cervical dilatation, and the delivery of the
fetus and placenta which corresponds to the clinical stages of labor
• Divided into three stages (see functional division/stages of!abor below)
First stage: clinical onset of labor up to full cervical dilation & effacement
Second stage: fetal descent and expulsion
• Third stage: delivery of placenta and membranes

IV.PHASE4: THE PUERPERIUM

• From delivery up to about 1 hour after delivery: myometrium remains contracted (which
compresses the uterine vessels and sinuses to prevent hemorrhage)
• Uterine involution and cervical repair happens to restore these organs to previous
non pregnant state
• During early puerperium, lactogenesis and milk let-down occurs
• Ovulation generally occurs 4-6 weeks after birth, though lactation can cause prolactin-
mediated anovulation
92
FUNCTIONAL DIVISION (STAGES) OF LABOR
The labor curve shown below incorporates the functional divisions of labor (i.e.,
preparatory, dilatational, and pelvic divisions) and the stages of labor {i.e., first and
second stages only are shown)
• Cervical dilatation (time versus cervical dilatation) follows a sigmoid curve (main phases
of which are the latent and active phase)
• Fetal head descent (time versus station of the head) follows a hyperbolic curve: maximum ■·
rate of fetal descent starts at 8 cm dilatation (corresponds to deceleration phase) ~ •
Engagement of the fetal head may occur before or at the onset of labor but further · ·•
descentoccurslateinlabor

-5

-4

8 -3
E
u -2
c· "T1
~ 6 -1 "'
g_
.,"'
.!!! ~
'a
;;;
0
...
QI

o·
u +1 ::s
-~
QI
4

u +2

+3
2
+4
dilatation
+5

PREPARATORY DILATATIONAL PELVIC

e
DIVISION DIVISION DIVISION

LATENTPHASE ACTIVE PHASE SECOND

STAGE
FIRSTSTAGE

• The preparatory division covers the latent phase of the first stage of labor up to the
acceleration phase of the active phase. The dilatational division is the same period as the
phase of maximum slope where the cervix dilates rapidly. The pelvic division begins at the
deceleration phase which is at 8 cm dilatation where cardinal movements occur since the
fetal head is already navigating through the pelvis
• The first stage of labor begins at the start of true labor and ends at 10 cm dilatation.
This stage is divided into latent (relatively flat) and active (rapidly progressive) phase.
Friedman initially pegged the beginning of active phase at 4 cm. But recently, Zhang, et al
already moved the active phase at 6 cm where rapid cervical dilatation is observed. The
second stage of labor begins at 10 cm or full dilatation until the baby is delivered which
normally lasts for 1 hour
Source:CunninghamFG, et al. WilliamsObstetrics25th Ed; 2018

93
Divisions of Labor
Functional Divisibns of Labor
Preparatory • Cervix dilates little but connective tissue components change
Division • Sedation and conduction analgesia can arrest this division
Dilatational • Cervical dilation proceeds at its most rapid rate
Division • Unaffected by sedation
• Commences with deceleration phase of cervical dilatation and includes
Pelvic
the second stage of labor
Division
• Cardinal fetal movements take place in this division
Phases df Cervica{ Dilatation
• Corresponds to the preparatory division
• Ends once dilation of 3-5 cm (Friedman) or 6 cm (Zhang) is achieved
Latent Phase • Prolonged latent phase
Nullipara: >20 hours
0

Multipara: >14 hours

0

I • Corresponds to the dilatational division

• Threshold for active labor: cervical dilation of 3-5 cm (Friedman) or 6
cm (Zhang) in the presence of uterine contractions
• Further subdivided into:
Acceleration phase
0

Active Phase Phase of maximum slope (measure of the efficiency of the machine)
0

Deceleration phase (measure of feto-pelvic relationships)

0

• Minimum rate of normal cervical dilation:

Nullipara: 1.2 cm/hr
0

Multipara: 1.5 cm/hr

0

• Descent commences at 7-8 cm for nulliparas

-
Stages ofLabor n
• Stage of cervical effacement and dilation
• Begins when spaced uterine contractions of sufficient frequency,
1st stage
intensity, and duration are attained to bring about effacement to full
cervical dilation
• Stage of fetal expulsion
2nd stage
• Begins with complete cervical dilation to fetal delivery
• Stage of placental separation and expulsion
3rd stage
• Begins immediately after delivery of fetus to placental delivery

Timeline of the Stages

I NULLIPARA I MULTI PARA

Duration of First Stage 8 hours 5 hours
Cervical dilatation 1.2 cm/hr 1.5 cm/hr
Descent 1 cm/hr 2 cm/hr
Arrest of dilatation >2 hours at the same cervical dilatation
Arrest of descent >l hour at the same fetal station
Duration of Second Stage 50 minutes 20 minutes

94
I. FIRSTSTAGE:CLINICAL ONSETOF LABOR(CERVICAL EFFACEMENT & DILATION)
• Time from onset of labor to complete cervical dilation
• Signs of labor initiation: spontaneous release ofa small amount of blood-tinged mucus
(heralded by mucus plug, "show" or "bloody show") from the vagina
Pushing or maternal intraabdominal pressure:
, Most important force in fetal expulsion
Contraction of the abdominal muscles simultaneously with forced expiratory efforts

■
with the glottis closed (as in valsalva maneuver)
Necessary to complete second-stage labor .

UTERUS DURING LABOR* I CERVIX DURING LABOR**

'The activeuppersegmentretractsaroundthe presentingpartas thefetusdescendsthroughthe birthcanal.In the

passivelowersegment,thereis considerablylessmyometrialtone
"This phaseis characterized by cervicaleffacement& dilation.Beforelabor,the cervixis longand undilated(in
primigravids)or minimallydilated(in multiparas)[AJ. Effacementthenbegins,showingdilationand funnelingof the
internalos [BJ. Completeeffacementanddilationis thenachieved(CJ.
Source:CunninghamFG,et al. WilliamsObstetrics25thEd;2018
A. Uterus
' Pain due to uterine smooth muscle during labor is due to:
• Hypoxia of the contracted myometrium
• Compression of nerve ganglia in the cervix and lower uterus
• Cervical stretching during dilatation (Ferguson reflex)
• Stretching of the peritoneum overlying the fund us

SEGMENT
OF UTERUS
I REMARKS

• Firm during contractions (contracts, retracts and expels the fetus)

Upper • Myometrium does not relax to its original length after contraction
segment • The upper active segment becomes progressively thickened throughout
the first- and second-stage labor
• Softer, distended, and more passive
• Cervix dilates and thereby forms a greatly expanded, thinned-out tube
through which the fetus can pass
Lower
• Physiological retraction ring: lower segment thinning and concomitant
segment
upper segment thickening
• Pathological retraction ring: also called Band! ring, happens when
thinning of the lower segment is extreme
95
B. Cervix
• Due to contraction forces, effacement and dilation occurs in the ripened cervix
• Canal must dilate to 10 cm in diameter for an average-sized fetal head to pass through the
cervix (i.e., "fully dilated")
• Effacement and dilation causes formation of the fore bag of amniotic fluid (leading portion
of fluid and amniotic sac located in front of the presenting part)
• Cervical effacement is "obliteration" or "taking up" of the cervix
Cervical • Shortening of the cervical canal from a length of ~3 cm to a mere circular
effacement orifice with almost paper-thin edges
• Causes expulsion of the mucous plug as the cervical canal is shortened
• Occurs due to a centrifugal pull exerted from the lower uterine segment
• The hydrostatic action of the amniotic sac or presenting part (if
Cervical
membranes are absent) dilates the cervical canal like a wedge
dilation
• Sigmoid curve is the pattern of cervical dilatation during the preparatory
and dilatational divisions of normal labor

C. Phases of the First Stage of Labor

• First stage of labor consists of two phases: latent phase and an active phase
• Although cervical softening & early effacement may occur before labor, the entire cervical
length is retracted into the lower uterine segment during the 1" stage of labor
PHASE I DESCRIPTION I REMARKS
• Duration is variable and sensitive to changes by
extraneous factors (e.g., sedation, myometrial
stimulation):
• Characterized by
• Excessive sedation or epidural anesthesia
gradual cervical change
Latent • Unfavorable cervical condition
• Onset of labor to about
phase ° False labor
4 cm (Friedman) or 6
• Has little bearing on subsequent course of labor
cm (Zhang) dilatation
• Prolonged latent phase:
• Nullipara: >20 hours
• Multipara: >14 hours
• Characterized by rapid
cervical change
• From 4 cm (Friedman) • Rate of cervical dilatation:
or 6 cm (Zhang) • Nullipara: 1.2 cm/hour
dilatation up to full • Multipara: 1.5 cm/hour
Active
dilatation • Factors affecting active phase duration:
phase
• Divided into: • Epidural anesthesia: prolonged labor curve
• Acceleration phase to 1 hour
• Phase of maximum • Maternal obesity: prolonged to 30-60 mins
slope
• Deceleration phase

96
II. SECOND STAGE: FETAL DESCENT
• Time from complete cervical dilation to fetal expulsion/delivery
• In many nulliparas, engagement of the head is accomplished before labor begins
• Vertex enters pelvis with the sagittal suture lying in the transverse pelvic diameter in the
majority of patients

-
• Uterine contractions effect modifications in fetal attitude:
° Fetal straightening
° Closer application of the extremities to the body

Cardinal Movements in the Vertex Position

• Mechanism of labor: series of movements that occur with the fetal head in the process of
adaptation during its passage through the pelvis
• Although the principal movements are in relation to the fetal head, the rest of the fetus is
also involved either by participating or initiating the motion
• Vertex enters the pelvis with the sagittal suture lying in the transverse pelvic diameter in
most cases (e.g., LOT in 40%)

CARDINAL
MOVEMENT
I PURPOSE
I REMARKS

• Mechanism by which biparietal diameter (widest transverse

• Demonstrate diameter) of fetal head passes through pelvic inlet
adequacy of • Biparietal diameter (BPD): the greatest transverse
Engagement
maternal bony diameter in an occiput presentation (passes through
inlet the pelvis usually either transversely or obliquely)
• In nulliparas, it may take place before onset of labor
• First requisite for birth of the newborn.
0 Nulliparas: descent may not follow until the onset of

the second stage

0 Multiparas: begins with engagement
• Most
• Descent begins at 8 cm in nulliparas
important
Descent • Descent is brought about by one or more of four forces:
component of
0 Pressure of the amnionic fluid
labor
0 Direct pressure of the fund us upon the breech with
contractions
0 Bearing-down efforts of maternal abdominal muscles

0 Extension and straightening of the fetal body

• Allows
narrowest • Flexion occurs as the descending head meets resistance,
AP diameter whether from cervix, pelvic walls, or pelvic floor
Flexion (suboccipito- • Chin is brought into contact with the fetal thorax
bregmatic) to • The shorter suboccipitobregmatic diameter is
present to the substituted for the longer occipitofrontal diameter
birth canal
97
CARDINAL
MOVEMENT
I PURPOSE

• Allowswidest
I REMARKS

• The occiput gradually moves toward the symphysis

diameter to
Internal pubis anteriorly from its original position (e.g., from
present to the
rotation LOTto OA;or from LOAto OA)
widest diameter
• Internal rotation is essential for completion of labor
of midpelvis
• Base of the occiput is in direct contact with the
• Directs the
inferior margin of the symphysis pubis
axis of the fetal
• Extension brought about by two forces:
Extension head upward
° Force exerted by the uterus (acts more posteriorly)
to the pelvic
° Force by the resistant pelvic floor and the
outlet
symphysis (acts more anteriorly)
• Allows the
• Rotation of the fetal body and serves to bring
transverse
its biacromial diameter into relation with the
External diameter of
anteroposterior diameter of the pelvic outlet
rotation fetal shoulders
• Occiput moves from occiput anterior back to its
(Restitution) to present the
original position during engagement (e.g., LOTor
widest diameter
LOA)
of the midpelvis
• Anterior shoulder appears under the symphysis
pubis, then the perineum becomes distended by the
• Completes the posterior shoulder
Expulsion birth process of • Gentle downward traction to deliver the anterior
the fetus shoulder is done, followed by upward traction to
deliver the posterior shoulder, then the rest of the
body is delivered

Pelvic inlet
plane

ANTERIORASYNCLITISM NORMALSYNCLITISM POSTERIORASYNCLITISM

• The head position is considered to have normal synclitism when the biparietal diameter is
parallel to the pelvic plane and the sagittal suture is midway between the symphysis and
the sacral promontory. When there is lateral deflection of the sagittal suture and parietal
bone, then there is asynclitism. If the sagittal suture approaches the sacral promontory
and more of the anterior parietal bone presents itself to the examining fingers, the
condition is called anterior asynclitism, and vice versa.
FG,et al. WilliamsObstetrics
Source:Cunningham 25thEd;2018

98
Ill. THIRD STAGE:DELIVERYOF PLACENTA& MEMBRANES
• Begins immediately after fetal birth and ends with placental delivery
• After the baby has been delivered, the uterus contracts, leading to a disparity between
size of placental surface & site of placental attachment (which is the reason for separation
of the placenta)

A. Signs of Placental Separation:

0

0
Sudden gush of blood
Uterus becomes globular (round) and firmer (Calkins sign)
Lengthening of the visible portion of the umbilical cord
Rise of uterus into the abdomen
I
.

B. Two Mechanisms of Placental Expulsion

SCHULTZE MECHANISM I DUNCAN MECHANISM
("ShinySchultze") ("Dirty Duncan")

• Placenta separates first at the periphery

• Blood collects between the membranes
• Blood from the placental site pours into
& uterine wall and escapes to and then
the membrane sac and does not escape
from the vagina
externally until after extrusion of the
• In this circumstance, the placenta
placenta
descends sideways, and its maternal
surface appears first

99
 SECTION THREE
INTRAPARTUM ASSESSMENT

ELECTRONIC FETAL HEART RATE (FHR) MONITORING

• Electronic FHR monitoring is commonly used to assess fetal well-being during labor
• Normal labor is characterized by regular uterine contractions, which cause repeated
transient interruptions of fetal oxygenation (most fetus tolerate this well, but some do not)
• Identification of FHR changes potentially associated with inadequate fetal oxygenation
may enable timely intervention

Components of the Report

• Baseline fetal heart rate (FH R)
• Variability (e.g., absent, minimal, moderate, marked)
• Presence or absence of accelerations or decelerations
• Interpretation (Category 1, 2, or 3)
• Frequency, duration, and strength of contractions

Sample Tracing

too,-+--~r ·t-FF=-==J=
r ♦-•-+ -t+--- - t=
"~-
!,(.It !- -t-t- -t- -1~:--
;-:t-rTi
--..-\.-- -:-:1* - ,-~- .! .. ( -+-+-·/,.•
'1---....-f-- "--" " -, ✓ i-- • -
4 •-,:\.--=-i=
"i:' .,+- :· ---,---• _, :::-r
,::j:::: 52 mmHg :!:EH 50 mmHg '3= 47 mm Hg ±d:± 44 mmHg =f d9mmHg ±
Speed oi tracing:1 cm/min
• Tracing A (upper figure) shows a normal or reactive FHR pattern expressed as beats per
minute (bpm). A small box corresponds to 10 fetal heart beats. In the example above, the
baseline FHR is about 120 to 130 bpm.
• Tracing B (lower figure) shows the uterine activity, which consists of the uterine
contraction pressure/intensity (0 to 100 mmHg) and contraction interval (interval
between the peak of contractions). The Montevideo Unit (MVU) can be computed using
this tracing. It is calculated by subtracting the baseline uterine pressure from the peak
contraction pressure for each contraction in a 10-minute window. In the tracing shown,
there are five contractions with contraction pressures of 52, 50, 47, 44 and 49 mmHg. The
sum of these contractions within the 10-minute period corresponds to the MVU.In this
case, the MVU is 242. Adequate uterine contraction is defined as 2200 MVU.
Source:CunninghamFG,et al. WilliamsObstetrics25th Ed;2018

100
BASELINE FETAL HEART ACTIVITY
• Refers to the modal characteristics that prevail apart from periodic accelerations or
decelerations associated with uterine contractions
• Includes rate, beat-to-beat variability, fetal arrhythmia, and distinct patterns such as

-
sinusoidal or saltatory fetal heart rates

I. BASELINEFETALHEART RATE (FHR)

• Mean FHR is rounded to increments of 5 bpm during a 10-minute tracing segment
• The minimum interpretable baseline duration should be at least 2 minutes
• Normal FHR baseline: 110-160 bpm

FINDING I DEFINITION I DIFFERENTIALS

Fetal • Congenital heart block
• Baseline FHR <110 bpm
bradycardia • Serious fetal compromise

• Most common cause: maternal fever from

chorioamnionitis
• Fetal compromise
Fetal
• Baseline FHR > 160 bpm • Cardiac arrythmias
tachycardia
• Maternal administration of parasympathetic
inhibiting ( e.g., atropine) or
sympathomimetic drugs (e.g., terbutaline)

II. BASELINEVARIABILITY
• Moment-to-moment or beat-to-beat oscillation (fluctuations) of the baseline fetal heart
rate that are irregular in amplitude and frequency
• Important index of cardiovascular function & is regulated by the autonomic nervous system
• Decreased variability is commonly caused by giving analgesic drugs during labor
• Reduced baseline heart rate variability is the single most reliable sign of fetal compromise
• Diminished variability <4.2 bpm maintained for 1 hour: diagnostic of developing
acidemia and imminent fetal death

DESCRIPTION I DIAGRAM

l_l~J~l_~l±tlil~~~--~
• Amplitude range is
Absent* undetectable (i.e.,
almost a straight line) t__
Minimal*
• Amplitude range is
,;5 bpm
lll!J•ll!~!lill
Moderate**
• Normal variability
• Amplitude range 6-25
bpm
Wrn#H#UIBI
Marked
• Amplitude range 2'25
bpm

-
'Conditionsassociated withabsent or minimalvariablityincludeextremeprematurity,preexistingneurologicinjury,
fetal sleep cycle, or medications
"Moderate baseline variability(preferred)reflectsthe oxygenationof the CNS and predictsthe absence of damag-
ing degrees of hypoxia-inducedmetabolicacidemia
Source:ArnoldKC,et al. ObstetricsEssentials;2017

101
III. SINUSOIDALOR SALTATORYHEART RATE PATTERN
• Visually apparent, smooth, sine wave-like undulating pattern in FHR baseline with a cycle
frequency of 3-5 bpm which persists for 2:20 min
• Observed with fetal intracranial hemorrhage, severe asphyxia, & severe fetal anemia

210

180
Characteristics:
~ C 150 • Stable baseline heart rate
~ .E of 110 to 160 bpm with
t
"'
a:; 120 / ' I/\ 1 I\ \I/ I\ i"\ regular oscillations

-
QJ C. I V
.c V,
• Amplitude of 5 to 15 bpm
"' "'
Q) QJ 90
I
(rarely greater)
u.. :3. • Long-term variability
60 frequency of 2 to 5 cycles
I
per minute
30 • Fixed or flat short-term
variability

-
V, 100
C ~ • Oscillation of the sinusoidal
0
.:; C waveform above or below
u ::, 75

~C 0
QJ
a baseline
0 'O
·;;; so • Absent accelerations
u
QJ
C
~
C
25
·~ 0
~
5

PERIODIC FETAL HEART RATE CHANGES

• Refers to increase (acceleration) or decrease (deceleration) in the baseline fetal heart
rate that are associated with uterine contractions and fetal movements

Overview of Terminologies
TERM I DEFINITION

• Abrupt increase (onset to peak in <30 seconds) in the FHR

Acceleration • Predicts the absence of damaging degrees of fetal hypoxia and fetal
academia
• Gradual (usually symmetrical) decrease and return of the FHR
associated with a uterine contraction
Early
• Nadir of deceleration occurs at the same time as the peak of contraction
deceleration
• Considered non-pathologic or benign
• May signify fetal head compression during a uterine contraction
Variable • Abrupt decrease in FHR
deceleration • May signify cord compression
• Gradual (usually symmetrical) decrease and return ofFHR associated
with a uterine contraction
Late
• Nadir of deceleration occurs after the peak of the contraction (i.e.,
deceleration
delayed in timing)
• May signify uteroplacental insufficiency
• Decrease in FHR below baseline that is >15 bpm & >2 minutes in
Prolonged
duration (but <10 minutes)
deceleration
• Interruption of fetal oxygenation occurs at a longer period of time

102
I. ACCELERATIONS
• Abrupt FHR increases above the baseline
0 At >32 weeks AOG:acceleration has a peak of?lS bpm from baseline, lasts for ?15 secs,
but <2 mins from onset to return to baseline
At <32 weeks AOG:acceleration has a peak of?l0 bpm from baseline, lasts for ?10 secs,
0

but <2 mins from onset to return to baseline

• Prolonged acceleration: defined as an acceleration that lasts ?2 mins, but <10 mins duration
• If acceleration lasts ?10 mins, it is a baseline change
.-------,-JO--~-
Ill
r--
I I
I
I I
Onse~ reak Onse~ Peak ~-- -+ I L
I
I I
I I
I I
I
I
I
I
I
I
1,---rP--H-+ - - - iAJ,
I
"'

~
'I I I

I -
60
! ' I
I

I
I ': I I I I
lO
I I I

100

"Thelinesshowthe onset and peak of the

accelerations,or transientincreases in FHR
fromthe baseline

II. EARLYDECELERATION
Visually apparent, usually symmetrical gradual decrease and return of the fetal heart rate
associated with a uterine contraction
Gradual FHR decrease: defined as from onset to FHR nadir of?30 seconds
0

The nadir of the deceleration occurs at the same time as the peak of the contraction
0

• It is "symmetrical": onset, nadir and recovery are coincident with the beginning, peak and end
of the contraction, respectively

~v
210 TIME
ONSET TO NADIR
~c
..
e? 'E
t'. -
• a.
.c -
180

!SO
~30:

~~
~£
110

90
I
I : :
l
100

C:vi 15
.g·E

ii.
C
·;:
~
C
0
so

,l:,
::,- "
Peak of contraction
Cause: Fetal Head Compression
• Uterine contraction causes transient fetal head compression leading to increased ICP and
reflex parasympathetic stimulation
• This causes gradual slowing of the FHR and early deceleration
• When head compression is relieved, autonomic reflexes subside and FHR returns to baseline
103
III. VARIABLEDECELERATION
• Visually apparent, abrupt decrease in FHR
0 Abrupt: from onset to FHR nadir of <30 seconds
The decrease in FHR is 2:15 bpm, lasting for 2:15 seconds but <2 mins duration
0

• Onset, depth, & duration of decelerations commonly vary with successive uterine contractions

::11111 """"
TIME

1:~T""
·················••········-············-\\0V
~----• A
Cause: Umbilical Cord Compression
Peak of contraction

• Umbilical cord compression causes initial compression of umbilical vein, leading to transient
decrease in fetal venous return. This leads to transient decrease in fetal cardiac output and BP,
causing baroreceptor stimulation and transient increase in FHR
• Umbilical artery compression causes an abrupt increase fetal peripheral resistance and BP,
causing baroreceptor stimulation and reflex parasympathetic outflow. This leads to abrupt
decrease in FHR causing variable deceleration
• When cord compression is relieved, the process occurs in reverse

IV. LATEDECELERATION
• Visually apparent, usually symmetrical gradual decrease and return of the fetal heart rate
associated with a uterine contraction
Gradual: from onset to FHR nadir of 2:30 seconds
0

The nadir of deceleration occurs after the peak of contraction

0

• Symmetrical: onset, nadir and recovery occur after the beginning, peak and end of the
contraction, respectively
I TIME
~c I ONSETTO NADIR
~ E ISO
I \
,:: C

~ ~ .I I
.c • •' '
~1
120
'I LATE :: ~30:

T
I I
I
90 '
''
100
'

75

A
~vi' '
.g ·"§ '
'
so '
eu o" '
§i '
'
~~
·;: 0
25
'
~:,
::,- '
Peak of contraction
Cause: Uteroplacental Insufficiency
• Common causes of uteroplacental insufficiency: placental dysfunction, maternal
hypotension following epidural anesthesia or excessive uterine activity
• Decreased uteroplacental oxygen transfer to the fetus leads to chemoreceptor stimulation
and triggers an alpha adrenergic response
• This causes fetal hypertension leading to baroreceptor stimulation and parasympathetic
response causing deceleration
104
V. PROLONGED DECELERATION
• Visually apparent decrease in FHR below baseline of lasting ;,2 but <lOmin
• lfthe deceleration lasts ;elOmin, it is a baseline change

210 r,-,---,-,-.-,-,---,-.-.--,-,--,.-.--,-,-.,-.--,-,-,,-,-r,,-,-,-r,,-,-T7

180 H-+-+-+-t-tl-+-+-+-t-t-+- IH-+-+-+-t-t-+-+-+-t-t-+-+-+-t--t-t-+-+-t--t-t-1

PROLONGED

"' ..
I
.

1 -+--+i-,,,-¥4c-.-+-"+-+~-
120 H-+-+-+-t-t-+-+--"'--+"'=..;...ch,JM...q>'--1~f'1'\.H- 1
Hv-+-l-+-H-+-+--+---l

90 >-+-t--+-+-+-<-t--+-+-+-<-+-t-+-+-<r-+-+--+-+-,r-+-+--+-+->-+-+--t-+-t--t-t--+-+-t

60 H-+-+-+-t-t-+-+-+-t-1-t-+-+-t-ir+-++-+-cr+-+-l--t-t-t-+-t-+-t-t-+-+--+---l

75

25

• Common causes: uterine hyperactivity, epidural, spinal, or paracervical analgesia, cord

entanglement, maternal supine hypotension

105
THREE-TIER FETAL HEART RATE INTERPRETATION SYSTEM
• Fetal heart rate (FHR) monitoring during labor is essential to determine if a fetus is well
oxygenated
• A three-tiered system for categorization of intrapartum FHR pattern is used
• This categorization evaluates the fetus only at that point in time
• The FHR tracing may move back and forth between these categories at any time during
labor, depending on the clinical situation

CATEGORY I FEATURES
• Strongly predictive of normal fetal acid-base status
• Can be followed-up in a routine manner without specific action

Normal • Baseline fetal heart rate: 110-160 bpm

tracings* • Moderate variability: amplitude 6-25 bpm
• No late or variable decelerations
• Presence or absence of early decelerations
• Presence or absence of accelerations
• Tracings may represent an appreciable fraction of those
encountered in clinical care
• Requires continued surveillance and reevaluation
• Baseline rate
0Bradycardia not accompanied by absent baseline variability
0Tachycardia
• Baseline variability
, Minimal baseline variability
0Absent baseline variability not accompanied by recurrent
Indeterminate decelerations
II
tracings** 0Marked baseline variability
• Periodic or episodic decelerations
0Recurrent variable decelerations accompanied by minimal or
moderate baseline variability
0Prolonged deceleration 2'2 mins but <10 mins
0Recurrent late decelerations with moderate baseline variability
0Variable decelerations with other characteristics, such as slow
return to baseline, "overshoots," or "shoulders"
• Accelerations
0Absence of induced accelerations after fetal stimulation
• Predictive of abnormal fetal-acid base status
• Sinusoidal pattern, or
Abnormal • Absent of baseline variability+ any of the following:
Ill
tracings** Recurrent late deceleration
0

Recurrent variable deceleration

0

Bradycardia
0

•Management
of CategoryI is routinemonitoring
.. Management of Categories II andIll aimto improvefetaloxygenationanduteroplacental bloodflow,stepsto
diminishuterineactivity,andreliefof umbilicalcordcompression. Potentialinterventions
arelateraldecubitus
positioning,
administering maternaloxygen,discontinue oxytocin,or amnioinfusion
for variabledecerations
Source:ArnoldKC,et al. Obstetrics
Essentials;
2017

106
 SECTION FOUR
INDUCTION AND AUGMENTATION OF LABOR
OVERVIEW OF INDUCTION AND AUGMENTATION OF LABOR
• Goal of induction & augmentation is to effect uterine activity sufficient to produce cervical
change and fetal descent, while avoiding development of a non-reassuring fetal status
• Indicated when benefits to mother/fetus outweigh those of pregnancy continuation
• Intervention designed to:

0
Artificially initiate regular uterine contractions
Progressively dilate and efface the cervix
I
'

0 Effect birth of the baby

• Pre-induction assessment:
Confirmation of parity & AOG Fetal presentation, estimated fetal weight
0 Bishop score Uterine activity
° Fetal well-being (e.g., BPS, NST) Indication for induction

I INDUCTIONVERSUSAUGMENTATION
OF LABOR
• Process whereby labor is initiated by artificial means
Induction of
• Stimulation of contractions before the spontaneous onset of labor, with
labor
or without ruptured membranes
• Effecting regular uterine contractions by artificial means in cases of
Augmentation spontaneous labor with irregular & inadequate uterine contractions
of labor • Stimulation of spontaneous contractions considered inadequate
because of failure of the cervical dilatation or descent of the fetus

II. BISHOPSCORE
• Quantifiable method used to predict labor induction outcomes
Bishop score of 9: high likelihood for a successful induction
• Bishop score of 4 or less: unfavorable cervix which may require cervical ripening
SCORE I DILATATIONI EFFACEMENT I STATION ICONSISTENCYI POSITION
0 Closed 0-30% -3 Firm Posterior
1 1-2 cm 40-50% -2 Medium Midposition
2 3-4cm 60-70% -1 Soft Anterior
3 ;,S cm ;,80% +1, +2 --- ---
Dilatation:averagediameterof cervicalopening
Effacement: degreeofdecreasein the cervicallength
Station:levelof presentingpartin relationto the ischialspine(station0)
Positionof the cervix:relationship
ofthe cervicalos to the fetalhead
• Posterior(lessfavorable):cervixpointedposteriorly
• Midposition (favorable):
cervixin midline
• Anterior(morefavorable):cervixpointedanteriorly
Source:Cunningham, FG.Williams Obstetrics25thEd1t1on,
2018and Bishop,1964
III. INDICATIONSAND CONTRAINDICATIONS
FORINDUCTIONOF LABOR
INDICATIONS I CONTRAINDICATIONS

• Gestational hypertension • Malpresentation (e.g., breech)

• Preeclampsia, eclampsia • Absolute cephalopelvic disproportion (CPD)
• Prelabor rupture of membranes (PROM) • Placenta previa
• Maternal conditions (e.g., OM, renal, APAS) • Previous major uterine surgery (e.g.,
• Gestation >41 ''' weeks classical CS,myomectomy)
• Fetal compromise (e.g., FGR) • Invasive carcinoma of cervix
• lntraamniotic infection • Cord presentation
• Fetal demise • Active genital herpes
• Logistic factors (e.g., history of rapid labor, • Conditions that preclude vaginal birth
proximity from hospital, psychosocial) • Physician's convenience
107
IV. PREINDUCTION CERVICAL RIPENING AND/OR LABOR INDUCTION REGIMENS

• Remain recumbent for at least 30 minutes

• Dinoprostone • Shorter 1-0 times with oxytocin infusion
cervical gel, • Contraindications: hypersensitivity, suspicion of CPD,
0.5 mg unexplained vaginal bleeding,women on oxytocinor with
Prostaglandin >6 term deliveries, contraindication to vaginal delivery
EZ
• Inserted in the posterior fornix
• Dinoprostone • Insert has shorter 1-0* times than gel preparation
insert, 10 mg • May start oxytocin at least 6-12 hours from last insert
• Remove if FHR abnormalities develop
• May be taken per orem (50-100 ug) or inserted per
Prostaglandin • Misoprostol
vagina (25 ug or 1/2 tablet)
El (off-labeluse) 100-200 ug**
• Contractions occur within 30-60 minutes
Mechanical
• Insert with balloon just above the internal cervical os
& infuse 30-mL sterile water to inflate the balloon
Transcervical foley catheter
• Improves Bishop scores rapidly
(French 36 with 30 mL balloon)
• With extra-amnionic saline infusion at 30-40 mL/hr,
results improve & possibly decreases infection rate
• Upper end of the tent is at the level of internal os
Hygroscopic dilators • Usually dilates within 12-24 hours after insertion
(Laminaria tent) • Rapidly improves Bishop score
• May shorten 1-0* times with oxytocin
'I-D: Induction-to-Delivery
"Misoprostolis not FDAapprovedfor usein thelocalsetting
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition,2018
V. METHODS OF LABOR INDUCTION
METHOD I REMARKS
Membrane • Manipulation of cervix & "stripping" fetal membranes is associated with a
stripping rise in prostaglandin F2a metabolites which may induce contractions
• Dosage: 10-units ofoxytocin (1-mL ampule) is diluted into 1 L crystalloid
(e.g., LR). This mixture results in a concentration of 10 mU/mL:
0 Low dose: starting dose at 0.5-1.5 mU/min; titrated every 15-40 mins at
increments ofl mU/min
0 High dose: starting dose at 4-4.5 mU/min, titrated every 15-30 mins at
Oxytocin
increments of 4-4.5 mU/min
• Discontinue if with signs of hyperstimulation or tachysystole:
0 5 contractions in 10 mins
0 Hypertonus: contractions lasting> 120 seconds
0 Excessive uterine activity with an atypical or abnormal fetal heart rate
• Commonly performed when labor is abnormally slow
0 Early amniotomy (1 to 2 cm): associated with reduction in labor
Amniotomy duration and increased incidence of chorioamnionitis
("surgical 0 Late amniotomy (5 cm)
induction"
• Fundal or suprapubic pressure may be applied during amniotomy to avoid
or the
artificial the risk of cord prolapse (some prefer doing it during a contraction)
rupture of • FHR is assessed before & immediately after amniotomy due to risk of cord
membranes) prolapse or rarely abruption
• Complications include chorioamnionitis, umbilical cord prolapse, cord
compression, FHR decelerations, or bleeding from fetal/placental vessels
108
 SECTION FIVE
MANAGEMENT OF-LABOR IN THE VERTEX POSITION
MANAGEMENT OF FIRST STAGE OF LABOR
• First stage of labor includes cervical effacement and dilation
• Average duration is 8 hours in the nulliparous and 5 hours in the multiparous
• Stage when the mother is transferred to the labor room for maternal and fetal monitoring
Basic Principles in the Mana.aement of the First Sta.ae of Labor
• Determine if mother is truly in labor (see criteria for the diagnosis of labor below}
I
.

• Perform abdominal examination to obtain the fundic height and perform the Leopold
maneuver to determine fetal presentation & fetal heart tones
• Unless contraindicated, do a vaginal exam under aseptic technique to determine cervical
dilation and effacement, presentation, station and asses the pelvis
• Monitor and document progress of cervical dilation and descent every hour once in the active
phase to diagnose abnormal labor (plot in a partograph)
• Monitor the vital signs at least every hour once in the active phase
• Monitor FHR & uterine activity regularly either by:
0 Auscultation after a contraction at least every 30 mins (low-risk) or 15 mins (high-risk)
0 EFM with tracing evaluated at least every 30 mins (low-risk) or 15 mins (high-risk)
• Anesthesia consultation should take place prior to admission
• Oral intake of modest amounts of clear liquids (e.g. water, pulp-free juices) may be allowed

I. DIAGNOSISOF LABOR
A. Criteria for the Diagnosis of Labor
• Uterine contractions* (1 in 10 mins; 4 in 20 mins) by direct observation or by electronic
fetal monitor (at least 200 Montevideo units or MVU)
• Documented progressive changes in cervical dilatation & effacement
• Cervical effacement of>70-80%
• Cervical dilatation >3 cm
•uterinecontractionswithoutcervicalchangesDOESNOTmeetthe definition
of labor.

B. True Labor versus False Labor

PARAMETERS
Character of contractions:
• Frequency
• Interval
• Intensity
Radiation of pain
Effect on cervical dilatation
Effect on effacement
Effect of sedation
I TRUE LABOR
• Regular
• Shorter
• Increases gradually
• Hypogastric/ lumbosacral
• Open and effacing
• Progressive
• No effect
I FALSE LABOR
• Irregular
• Long, but may disappear
• Variable, but may disappear
• Mostly hypogastric
• Usually long and closed
• Does not occur
• May stop contraction

II. MONITORINGUTERINE CONTRACTIONS

• Determine time & onset of a contraction which is perceived as abdominal tightening
• Intensity is classified as mild, moderate or strong
• Duration, interval and frequency of contractions are monitored at intervals of 15-30 mins
CONTRACTIONS I EARLY LABOR I ACTIVE LABOR
• Every 3-5 mins initially, becoming
Frequency • Every 5-10 mins
more frequent as labor progresses
Duration • 30 seconds • 60-90 seconds
Intensity • Mild • Moderate to strong
109
III. FETALHEART MONITORING
• Fetal heart tones (FHT) may be evaluated by a stethoscope, doppler device, or electronic
fetal monitoring (EFM)
• Electronic fetal monitoring (see Section 3) monitors fetal heart tones and their
relationship to uterine contractions
• Since a uterine contraction is a form of stress on the fetus, the fetal heart rate taken after
a contraction may uncover early signs of fetal distress
0 Normal fetal heart rate is 110-160 bpm
Fetal compromise suspected when FHT is <100 bpm after a contraction and a drop
<100 bpm even in the presence ofa recovery rate between 110-150 bpm

High risk women • Every 15 mins • Every 5 mins

Source:AGOG;1995
IV. ATTENDANCE IN LABOR
• Monitoring FHT and uterine contractions need close observations
• The ideal set-up is 1 birth attendant is to 1 patient ratio

• In early stages, mother is allowed to ambulate or assume any comfortable

position
Maternal
• Left lateral decubitus: may be a resuscitive measure to improve fetal
position
blood flow
during labor
• Restriction of activity is done in cases of ruptured membranes to prevent
occult cord prolapse or when maternal sedation has been instituted
Subsequent • Timing is based on uterine contractions
vaginal • Limit internal examination in cases of early rupture of membranes to
examination prevent chorioamnionitis
• Monitored hourly during the active phase of labor, early rupture of
Maternal
membranes, borderline temperature elevation or high-risk pregnancy
vital signs
• Blood pressure is preferably taken after a uterine contraction
Analgesia • Initiated on the basis of discomfort of patient who is in the active phase
• To find out the character of the amniotic fluid (to say if there is fetal distress)
• Spontaneous rupture of membranes is associated with a shortened
Amniotomy
duration of labor when compared to amniotomy or delivery with intact
membranes
• Patients with additional risk factors for aspiration (e.g., morbid obesity,
Oral intake DM,difficult airway) or at increased risk for operative delivery (e.g., non-
and IV fluids reassuring FHR pattern) may have further restrictions of oral intake
• IV fluids should not be given routinely

V. ACTIVE MANAGEMENTOF LABOR

• Includes amniotomy upon detection of painful uterine contractions with passage of bloody
mucoid discharge or complete cervical effacement, regardless of cervical dilatation
• Oxytocin infusion is started if dilatation does not progress, at least 1.2 cm/hr in
primigravida or 1.5 cm/hr in multigravida, to augment labor (increase uterine
contractions in women in labor)

110
VI. WORLD HEALTH ORGANIZATION (WHO) PARTOGRAPH
• Used to record all observations made on a woman in labor in low-resource settings
• It aids the primary health care giver in a primary health facility (health center) to
determine whether there is a need to transfer the patient to a tertiary center

Features of the WHO Partograph:

• Fetal heart beat is plotted at regular intervals
• Used when the cervical dilatation is> 4 cm (active phase)

■
• Expected rate of cervical dilation is 1 cm/hour, regardless of gravidity
.
• Normal cervical dilatation should fall within the ''ALERT"line
• If cervical dilation crosses the ALERTline, then there is a need to transfer to a tertiary facility

Some Examples
Cervical dilation not crossing Alert Line
Name Gravida Para Hospital Number
Date of Admission Time of Admission Ruptured membranes Hours

10
9 V
v ,,,.,,,,,,,I
1,,,./ I ,,,,v
I/
/

8
i,,,:...,_~
./ ./ ,o'1' ,,,.v
7
k"'~ /./ .,.c-v
./
6 - p
IJ v/ / /

1:
Descent of ,,i,.
ro,
V
V / /

Fetal head (Plot 0) 2 r-,..

1 ""r-,.
I 0 ..........

HT~::1
12
111111111111111
1 2 3 4 5 6 7
IIIIIIIII
8
PM PM PM PM PM PM PM PM PM

Cervical dilation crossing Alert Line

Name Gravida Para Hospital Number
Date of Admission Time of Admission Ruptured membranes Hours

10 !// //
9 I 1,,,,V ,, I I v"'
8
,_'<.¢-/~ .... ,o'1' ,/
V

7 ,,,I" i,.◊ V
/
6
,~i,..-°// I//

1; .,,v v"'
Descent of 3
Fetal head (Plot 0) ,.
~ ..........
-
1
I 0
~~
~

H~::1111111111111111
12 1 2 3 4 S 6 7
IIIIIIIII
8
PM PM PM PM PM PM PM PM PM

111
Cervical dilation crossing Alert Line but not crossing Action Line
Name Gravida Para Hospital Number
Date of Admission Time of Admission Ruptured membranes Hours

10 1,,..V IY ,,/
t-t-t-t-t-t-
I i,,,v l.,r'I r ,,/
,.-..----1r--t-t-t-+-+---1
8 <. ,/ 1 .,,...... I /
1>-'-::,
/ ,,.... c-'o~,.,/+--+--+--+-+-+-+--+--+--+
7 / i.,I"" I>',,/
6- -
// ~......... //
,,C+-+-+--+--+--+-+-+-+--+--+--+

1 5 ,,,,... ,v
41'11""1/4----,c......1-1-1-1-+-+"/+-+-+--+--+--+-+--+---+--+--+--,--+-I-!--,
'
Descent of '"fflc::t--t----+-+-+--+--1-r-r-t-+-+-+-+-+-+-t--t----t---t----t--t-+-I

Fetal her (Plot O) ~ l-~-t-..._-t-...,-t--+--+--+-ll--f----t-..,r-.._-3111,,..,lrrr-.._-!--t--+-t--ll--l--l-l-t-t-+-+-I

HT~::1
12
I I I I I I I 11111111111111111
1 2 3 4 6 7 8
PM PM PM PM PM PM PM PM PM

Cervical dilation crossing Action Line

Name Gravida Para Hospital Number
Date of Admission Time of Admission Ruptured membranes Hours

10 // ,_,/
9 I 1,,,,,, ,,v
8
,.,¢-// V
7 1>-"
Cervix (cm) ,,,..✓ i...,, ~ / /
(PlotX) 5--
c-'o;,,,
// I,,, ~ I>'/
....
1:
Descent of 3 '
_/.,:;. ,../

Fetal head (Plot 0) ,.

1
~ ........
I 0
r- r-,..
--
H~::1I I I I I I I I I 111111111111111
12 1 2 3 4 5 6 7 8
PM PM PM PM PM PM PM PM PM

112
MANAGEMENT OF THE SECOND STAGE OF LABOR
• Second stage of labor starts when cervix is fully dilated up to the delivery of the fetus
• At the time of full dilatation, the parturient (woman in labor) feels the urge to bear down
• Average duration of this stage is 50 mins for nulliparas and 20 mins for multiparas

Basic Principles in the Management of the Second Stage of Labor

• Parturient is placed in dorsal lithotomy position. Ensure that the legs are comfortably

■
placed on the stirrups. Bed is elevated to >45 degrees or Fowler position
.
• Asepsis and antisepsis is done
• Sterile drapes are placed
• Bladder drained with straight catheter
• Fetal heart tones are noted after every contraction every 15 minutes
• Patient is encouraged to bear down during a uterine contraction. She can bear down as
long as she is able and exhale slowly. Rest between contractions.
• Once fetal head reaches the perineum and the scalp is seen with a diameter of 2-3 cm,
episiotomy is done after administering adequate anesthesia
• The perineum is supported with one hand using a hand towel (Ritgen maneuver) and the
other hand tries to keep the head flexed to control delivery of the baby
• Once head is delivered determine for presence of nuchal cord and either slip it over the
shoulders or cut between 2 clamps. Clear baby's nose and mouth.
• Await external rotation or assist by bringing shoulders into anterior posterior position
• Deliver anterior shoulder by gentle downward traction followed by upward traction to
deliver posterior shoulder
• Gently deliver rest of the baby
• Apply the Essential intrapartum Neonatal Protocol (EINC): immediate drying of the baby,
skin-to-skin contact, timely cord clamping, and non-separation for early breastfeeding

I. PREPARATIONFOR DELIVERY
A. Delivery of the Head
0 With each uterine contraction, perinea] opening becomes ovoid to circular with
progressive dilatation
0 Perineum is stretched to paper-thin and rectal opening may also stretch
° Crowning is when the fetal head is seen encircled by the vulvar ring
° Failure to perform an episiotomy at this point invites perinea! lacerations
0 See cardinal movements of labor discussed in Section 2

B. Modified Ritgen Maneuver

0 By the time vulvar opening reaches a diameter of 5 cm, a towel-draped hand should be
used to exert forward pressure on the chin of the fetus through the perineum
0 The other hand is placed on the occiput and exerts pressure at this point
0 Head is delivered slowly with the base of the occiput, using the symphysis as a fulcrum
0 This maneuver allows control of the delivery of the head with extension and prevents
extension of the previously effected episiotomy

113
II. EPISIOTOMY
• An incision into the perineum to enlarge the space at the outlet, thus facilitating the birth
of the child
• Restricted use is preferable to routine use
• Median episiotomy is the first choice for episiotomy (but mediolateral episiotomy may be
preferable in selected cases, such as big babies, short perinea! body, and forceps delivery)

A. Indications to do an Episiotomy
' Expedite delivery in the 2nd stage of labor
' When spontaneous laceration is likely
' Maternal or fetal distress
' Breech position
0Assisted forceps
0Large baby
, Maternal exhaustion

B. Comparison Between the Types of Episiotomy

I MEDIAN (MIDLINE)
EPISIOTOMY
I MEDIOLATERAL
EPISIOTOMY

~ ~

Diagram

~£
• Begins at the fourchette
continuing to the perinea!
• Begins at the midline of the
fourchette and is directed
Description body at the midline and ends
to the right at an angle 60
before the external anal
degrees off the midline
sphincter is reached
• Done if perinea] body is long
• Done if perinea! body is short
Characteristics enough
• Likely to cut blood vessels
• Less chance to cut blood vessels
Surgical repair • Easy • More difficult
Healing • Good healing • Prone to faulty healing
Postoperative
pain • Minimal • Common

Anatomic result • Excellent • Occasional faulty

Blood loss • Less • More
Dyspareunia
• Rare • Occasional
(painful coitus)
Extension to the
anal sphincter & • Common • Uncommon
rectal mucosa

114
MANAGEMENT OF THE THIRD STAGE OF LABOR
• Starts from the delivery of the baby up to the delivery of the placenta
• Goals include the following:
0 Delivery of intact placenta
0 Avoidance of postpartum hemorrhage & uterine inversion
• Separation of the placenta usually occurs within 5 mins of delivery

__________ _, ■
~B_a_s,_·c_P_r_in_c,.:..·p_le_s_,_·n_t_h_e_M_a_n...;ag:::.....em_e_n_t_o::..f_th_e_T_h_ir_d_S_t_a-=g-e_o.:..f_L_a_b_o_r
• Await for signs of placental separation
• Do controlled cord traction. Place hand below fundus facing the mother's head. Push
fund us upward while placing gentle traction on the cord with opposite hand. As the
placenta reaches the perineum, slightly lift the cord
• Deliver placenta, slowly rotating as you pull
• Inspect placenta for completeness
• Massage fund us until contraction is felt. Start on oxytocin drip or give ergot derivatives, if
not contraindicated
• Inspect for lacerations. Do repair of episiotomy or lacerations
• Check for hematoma formation and integrity of the anal sphincters

I. UTEROTONICDRUGS
UTEROTONIC DRUGS I REMARKS
• Effective first line prophylactic uterotonic
• Safe to use on all patients
Oxytocin
• Lesser unpleasant side effects (e.g., nausea, vomiting &
hypertension)
Oxytocin analogues
• Synthetic analogue of oxytocin with a longer duration of action
(e.g., Carbetocin) -

• Second-line agents for prevention of postpartum hemorrhage

Ergot alkaloid (e.g.,
• Avoided in hypertensive and asthmatic patients
methylergonovine)
• Deteriorates rapidly with exposure to light, heat and humidity
• Not available for use in the country
Prostaglandin E • Considered inferior to oxytocin for prevention of postpartum
analogue (e.g.,
hemorrhage
Carboprost,
• Used in the absence of other uterotonics especially in resource-
Misoprostol*)
poor setting lacking oxytocin
'Misoprostolis not FDAapprovedforuse in the localsetting

II. MANUALEXTRACTIONOF THE PLACENTA

• Prolonged third stage oflabor (normal duration is 5 minutes) occurs when the placenta
does not separate promptly
• In the absence of bleeding. expectant management of 15-. 30- or up to 60-minutes may be
done before performing manual removal of placenta
• Three possibilities for placenta not being delivered immediately:
Placenta adherens: uterine connections insufficient to detach placenta
0 Lower uterine segment constriction and a detached but trapped placenta
0 Morbidly adherent placenta (accreta/increta/percreta)
• If placenta still remains attached for a prolonged period of time after delivery of the fetus,
there is increased risk of hemorrhage

A. Indications for Manual Extraction of the Placenta

Alarming hemorrhage of the third stage of labor
0

Placental retention ( >30 minutes)

0

115
B. Techniques in Manual Extraction of the Placenta

1 Generalanesthesia • Provides analgesia

• A full bladder can
2 Empty bladder interfere with the
placental delivery
Introduce
• Follow the umbilical
3 dominant hand
into the vagina cord up to the uterus

Move fingers of • Look for the edge of

the hand laterally the placenta (note
4 until the edge of that the cord attaches
the placenta is to the central portion
located of placenta)

Keep fingers • If there is difficulty

together and in detachment,
5 use them to stop! Think of
detach the placenta accreta (do
placenta hysterectomy)

• Use the ulnar side of

Create a space the hand to perform
between this procedure
6 placenta and • Fundal massage may
uterine wall promote tonic uterine
contraction

• Perform by carefully
Feel if the proceeding slowly all
placenta has
around the placental
7 been peeled or
bed until the whole
detached from
the uterine wall placenta has been
detached

Palpate uterine
cavity to ensure
8 complete
removal of • One complications is
placental tissue
incomplete placental
delivery
• Cotyledons must be
Examine the complete
9 placenta and
membranes

Consideradministeringoxytocin,whichfavorsuterinecontraction
andstopsbleeding
Thingsto remember:
• Donotexerttractiononthecordandtheplacentaseparately
• Donotmassage theabdomen
• Donotinfuseoxytocintoomuch(it cancauseretraction of theplacenta)
Source:SOGC.ALARMCourseSyllabus.Postpartum Hemorrhage; 2010
Source:Cunningham
FG,et al. WilliamsObstetrics
25thEdition;2018
116
III. INSPECTION OF THE VAGINA & PERINEUM FOR LACERATIONS
A. Types of Lacerations
FIRST SECOND THIRD FOURTH
INVOLVEMENT

Fourchette
I DEGREE
✓
I DEGREE
✓
I DEGREE
✓
I DEGREE
✓

Perineal skin ✓ ✓ ✓ ✓

■
Vaginal mucosa ✓ ✓ ✓ ✓ .

Fascia --- ✓ ✓ ✓

Perinea!body muscles ... ✓ ✓ ✓

Anal sphincter --- --- ✓ ✓

Rectal mucosa ... ... ... ✓

Firstdegree:tearonlypenetrates
vaginallining
Seconddegree(mostcommon): tearpenetrates thevaginallining& underlying
vaginaltissues
Thirddegree:tearextendsthroughvaginallining/tissues
andpartof theanalsphincter
Fourthdegree:tearextendsthroughvaginallining/tissues,
analsphincter,andrectallining
B. Performing the Episiotomy Repair
MEDIAN EPISIOTOMY REPAIR I MEDIOLATERAL EPISIOTOMY REPAIR

;M C
D~/

A.Ananchorstitchis placedabovethewoundapexto A. Vaginalepithelium anddeepertissuesareclosed

begina running, lockingclosure witha 2--0sutureto witha single,continuous,lockingsutureStartwith
dosethevaginalepithelium anddeepertissuesand a sutureabout1cmproximalto theapexof the
reapproximate thehymenal ring.Startwitha suture-1 lacerationwithinthevagina.Securethe suturewith
cmproximal to theapexof thelaceration withinvagina. a knot.Proceedwithcontinuous interlocking sutures
Securesuturewitha knol Proceed withcontinuous upto the levelof the hymenalring.
interlockingsuturesupto levelof hymenalring. B. Deeperperinea!tissuesarereapproximated by
B.A transitionstitchredirectssuturingfromvaginato singlecontinuous, nonlocking
sutureNext,suture
theperineum. Closethe hymenalringin a nonlocked thedeeperperinea!tissueswithsingle,continuous,
fashion.Tuckthissuturethroughthe hymenalring nonlocking sutures.Then,suturetogetherthe
andoutto the perinea!body musculartissueof the perinea!body(superficial
C.Superficialtransverse & bulbospongiosus muscies are transverse perinea!andbulbospongiosus muscles)
reapproximated usingcontinuous, nonlocking technique. usingcontinuous nonlocking
sutures.Closethe skin
Suture together muscular tissueof perinea!
body(supert'~ of theperinea!bodywithsubcuticular stitching
cialtransverseperinea!&bulbospongioous muscies) using C. Superficial
transverse andbulbospongiosus
continuous nonlocking sutures musclesarereapproximated usingcontinuous,
D.Thecontinuous sutureisthencarriedupwardasa nonlocking technique
subcuticular stitch.Whensuturereaches apexofthe D. Perinea!skinis closedusingsubcuticular stitch
wound, canyItbackupwards asa subcuticularstitch.End
witha finalknottiedatthelevelof hymenal ring.
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition,2018
117
MANAGEMENT OF THE FOURTH STAGE OF LABOR
• The hour after delivery of the placenta is a critical period wherein postpartum
hemorrhage as a result of uterine relaxation may occur
• Postpartum hemorrhage is discussed further in Chapters 6 and 7

Basic Principles in the Management of the Fourth Stage of Lobar

• Postpartum hemorrhage as a result of uterine relaxation may occur
• Maternal vital signs are checked frequently every 15 to every minute
• Gentle uterine massage will stimulate contractions and oxytocin may be infused. Firmness
of uterus is assessed periodically
• Bladder should be emptied
• Manipulation of the uterus must be done aseptically
• Intrauterine clots should be evacuated because it may impede effective uterine contraction

REFERENCES
!.American Academyof Pediatricsand the AmericanCollegeof Obstetriciansand Gynecologists: Guidelinesfor PerinatalCare,
8th ed. Elk Grove Village, MP, 2017
2.AmericanCollegeof Obstetriciansand Gynecologists. Fetalheart rate patterns:monitoring.interpretation,and management
ACOGtechnical bulletin 207, 1995
3.Arnold, K. C., & Flint, C. j. (2017). lntrapartum fetal heart rate monitoring: Nomenclature, interpretation, and general
managementprinciples.In ObstetricsEssentials(pp. 101-107). Springer;Cham.
4.Cunningham,F.G.,Leveno,K.]., Bloom,S. L.,Spong.C.Y..Dashe,J.S.,Hoffman,8. L.,Sheffield,J.S. (2018). Williams obstetrics
(25th edition.).New York:McGraw-HillEducation.
5.Eberle RL,Norris MC, EberleAM, et al: The effectof maternal positionon fetal heart rate during epidural or intrathecallabor
analgesia. Am J Obstet Gynecol 179:150, 1998
6.FreemanRK,Garite TH, NageotteMP: FetalHeart RateMonitoring,3rd ed. Philadelphia,LippincottWilliams & Wilkins, 2003
?.GilstrapLC111, Hauth JC.HankinsGD,et al: Secondstagefetal heart rate abnormalitiesand type of neonatalacidemia.Obstet
Gynecol 70:191, 1987
8.Hobel CJ, Zakowski M. Normal labor,delivery,and postpartum care. Obstetricsand Gynecology.Availableonline: https://
clinicalgate.com/normal-labor-delivery-and-postpartum•care/
9.https://www.perinatology.com/Fetal%20Monitoring/lntrapartum%20Monitoring.htm
10. littps:/ /www.youtube.com/watch?v=un3HxiD3BUQ
11. KentonK, Mueller M: Episiotomyand obstetricanal sphincterlacerations.In YeomansER. Hoffman BL,GilstrapLCIII, et al
(eds): Cunninghamand Gilstrap'sOperativeObstetrics,3rd ed. New York,McGraw-HillEducation,2017
12. Murata Y,Martin CB,lkenoueT, et al: Fetalheart rate accelerationsand late decelerationsduring the courseof intrauterine
death in chronicallycatheterizedrhesusmonkeys.Am I ObstetGynecol144:218, 1982
13. National Institute of Child Health and Human Development ResearchPlanning Workshop: Electronic fetal heart rate
monitoring:researchguidelinesfor integration.Am JObstetGynecol177:1385, 1997
14. Paul RH, Snidon AK, Yeh SY:Clinical fetal monitoring. 7. The evaluationand significanceof intrapartum baseline FHR
variability. Am I Obstet Gynecol 123:206, 1975
15. Smith JH,Anand KJ,CotesPM, et al: Antenatal fetal heart rate variation in relation to the respiratoryand metabolicstatus
of the compromised human fetus. BJOG95:980, 1988
16. SOGC.(2010) Advances in Labour and Risk Management Textbook (ALARM)Course Syllabus. Postpartum Hemorrhage.
SOGC.Ottawa, Ontario
17. Yang M, Stout MJ, Lopez JD, et al: Association of fetal heart rate baseline change and neonatal outcomes. Am J Perinatal
34(9):879, 20 I 7
18. Young BK,Weinstein HM: Moderate fetal bradycardia. Am J Obstet Gynecol 126:271, 1976

118
DYSTOCIA
(ABNORMAL
LABOR)
 SECTION ONE
MECHANISMS OF DYSTOCIA

REVIEW OF NORMAL LABOR

• In normal labor, uterine contractions cause progressive dilation and effacement of the
cervix, accompanied by descent and eventual expulsion of the fetus
• Normal labor progress is generally slower in nulliparous women
• Factors influencing progress of labor: uterine contractions, cervical resistance and

--~-o-rw_a-rd_p_r_es_s_u_r_e_e_x_e_r-te_d_b_y-th_e_le_a_d_i_n~g-fe_ta_l_p_a-rt---~-------------,
..I. THE DIVISION AND PHASES OF LABOR (Friedman Curve)
■.·
-5

-4

8 -3
E
u -2
c'
.g
J3
6
-1 ..
....
g_
.!l! a
'5 ~
"iii
.!:!
er
+1 ::,

..
C:
u
4
+2

+3
2
+4

+5

PREPARATORY DllATATIONAL PELVIC

e
DIVISION DIVISION DIVISION

lATENTPHASE ACTIVEPHASE SECOND

STAGE
FIRSTSTAGE

• First stage: time from onset of labor (contractions ;,200 MVU,every 3-5 mins) up to full
cervical dilatation (10 cm)
0 Latent phase: characterized by gradual cervical change, which begins with perception of
contractions from closed cervix up to 4 cm (Friedman) or 6 cm (Zhang)
0 Active phase: characterized by rapid & predictable cervical change from 4 cm
(Friedman) or 6 cm (Zhang), up to full cervical dilatation (10 cm)
• Second stage: time from complete cervical dilation to fetal expulsion
• Third stage (not shown above): time from fetal expulsion to placental expulsion

Timeline of the Stages

I NULLIPARA
I MULTIPARA

Duration of First Stage • 8 hours • 5 hours

Cervical Dilatation* • 1.2 cm/hour • 1.5 cm/hour
Descent • 1 cm/hour • 2 cm/hour
Arrest of Dilatation • >2 hours • >2 hours

Arrest of Descent • >l hour • >1 hour

Duration of Second Stage • SO minutes • 20 minutes

'Transitionfromthe latentto activephase occursat 4 cm cervicaldilationand the minimumrate of cervicaldilation
duringthe activephase is 1.2cm/hrfor nulliparouswomenand 1.5cm/hrformultiparouswomen

121
II. NORMALLABOR USING DIFFERENTPARTOGRAMS

I FRIEDMAN CURVE
I ZHANG CURVE
I WHO PARTOGRAPH
• Improve labor
management in
developing countries
• Define normal labor • Prevent premature • Intended for GPs
Purpose
progress cs and paramedical
personnel to know
when to refer to OB-
Gyn specialists
• Sigmoid curve • Exponential staircase
Shape of
• Slow cervical dilation line
labor curve • Diagonal straight
until ~4 cm, followed • Increase in cervical
(cervical lines
dilatation) by an abrupt dilation is more
acceleration gradual
• Active phase starts
• Active phase starts • Active phase starts at4cm
at 4 cm at6 cm • After line starts at 4
Progression , 1.2 cm/hr for • Progression is slow cm, action line is 4
pattern nulliparas before 6 cm hours from alert line
, 1.5 cm/hr for • Duration is <4 hours • Cervical dilatation
multi paras after 6 cm during the active
labor is 1 cm/hr

DYSTOCIA ("DIFFICULT LABOR")

• Also called dysfunctional labor, ineffective labor, failure to progress (dilatation & descent)
• Clinicians must rely on a trial of labor to determine if labor can be successful in effecting
vaginal delivery
• Abnormal labor alerts the physician to consider other methods for a successful delivery

I. MECHANISMSOF DYSTOCIA
• Abnormal progress of labor (spontaneous, induced, or augmented) related to the 3 P's:
Uterine factors (power)
, Fetal factors (passenger)
Bony pelvis (passage)

FACTOR
I REMARKS
I SOME CAUSES

• Hypo- or hypertonic uterine activity

• Uterine contractility
.f ower and maternal
expulsive effort
• Presentation, position
f assenger or development of the
fetus
• Pelvis and lower
_f assage reproductive tract
• Advanced maternal age
• Maternal obesity
• Neuraxial anesthesia
• Tocolytics, uterine relaxants
• Cephalopelvic disproportion (CPD)
• Non-occiput anterior position
• Large for gestation or macrosomia
• Contracted pelvic planes/diameters
• Short stature (<150 cm)
• High station at full dilatation
Source:MylesTD,ObstetGynecol;2003

122
II. GENERALMECHANISMS
• Most common etiology of dystocia is cephalopelvic disproportion (CPD)
Cephalopelvic disproportion: fetal head that is large on a small pelvis or abnormal fetal
head position on a normal or small sized pelvis
Fetopelvic disproportion: disparity of the size of the fetus for a small pelvis
• Hypocontractile uterine activity is the most common risk factor for protraction and/or
arrest disorders in the first stage of labor
MECHANISM I REMARKS I FEATURES
• Relationship between the power and the • Protracted labor: slow

I
passenger progress
• Uterine dysfunction can result from • Arrested labor: no
Uterine
overdistention, obstructed labor, or both progress
dysfunction
• Fetopelvic disproportion can also cause • Inadequate expulsive
uterine dysfunction effort: ineffective
• Can be managed medically pushing
• Relationship between passenger &
• Excessive fetal size
passage (i.e., disparity between fetal head
Cephalopelvic • Inadequate pelvic
and maternal pelvis)
(fetopelvic) capacity
• More apparent once 2nd stage is reached
disproportion • Malpresentation or
(CPD) • Ineffective labor is generally accepted as a
position of the fetus
possible cause of fetopelvic disproportion
• Abnormal fetal anatomy
• Managed by cesarean section (CS)
Source:Cunningham,FG.WilliamsObstetrics25thEdition;2018

III. COMPLICATIONS OF DYSTOCIA

A. Maternal Complications
• Intrapartum chorioamnionitis or postpartum pelvic infection
Infection
• More common with desultory and prolonged labors
Postpartum
• Due to uterine atony with prolonged and augmented labors
hemorrhage
Uterine tears
• May occur if the fetal head is impacted in the pelvis
with hysterotomy
• Particularly in women with high parity and in those with a prior
Uterine rupture
CS delivery
Pathological Band! • Associated with marked stretching & thinning of the lower
retraction ring uterine segment
• Pressure necrosis (due to impaired circulation from prolonged
Fistula formation 2nd stage) can become evident after several days as a
vesicovaginal, vesicocervical, or rectovaginal fistula
• Due to direct compression from the fetal head and to downward
pressure from maternal expulsive efforts
0 These forces stretch and distend the pelvic floor, resulting in
Pelvic floor injury
functional and anatomic alterations in the muscles, nerves, and
connective tissues
• May affect urinary or anal continence and pelvic support
• Due to prolonged second-stage labor
Lower extremity • Most common mechanism: external compression of the common
nerve injury fibular nerve due to inappropriate leg positioning in stirrups
especially during prolonged second-stage

B. Perinatal Complications
Fetal sepsis rises with longer labors
° Caput succedaneum and molding develop
0 Mechanical trauma such as nerve injury, fractures, and cephalhematoma
123
DIAGNOSIS OF ABNORMAL LABOR
I. ABNORMALLABORCRITERIAFOR DIAGNOSIS

~
p repa,:a ory D IVISlf?l!g
ABNORMAL LABOR CRITERIA FOR DIAGNOSIS

Prerequisite before diagnosing ''failed induction of labor:"

• There is an acceptable indication for induction (e.g., preeclampsia)
• Bishop score should be ;,5 prior to induction with oxytocin (if score is ,;4,
then cervical ripening must be employed until a score of 5 is achieved)

Failed induction of labor, defined as:

Latent • Remains in the latent phase (Friedman: <4 cm, or Zhang: <6cm),
1-3cm
Phase ruptured bag of waters with adequate uterine contractions (.e200
MVU), and at least 12 hours of oxytocin administration, OR
• Induction of labor with intact bag of waters due to difficult
amniotomy or other safety issues (e.g., presence of Group B
: Streptococcus) with adequate contractions for a duration of 12-,
15-, 18-, or 24-hours, depending on the clinical judgement of the
clinician. There is no consensus as of this writing
Early active • Arrest disorders will not apply in this phase
phase • In the presence of a protraction, reassess the 3 P's and manage
4-Scm (latentphase): expectantly or augment with oxytocin if needed
acceleration • If CS is decided, indicate the reason in the operative record (e.g.,
phase CPD, pelvimetry findings, fetal/maternal indications)

Dilatti'tional Dlvisio~ .,

True active • Active phase arrest is defined as cervix of .e6 cm with ruptured bag
phase: of waters with no cervical dilatation for:
6-7cm phase of • ;,4 hours with adequate uterine contractions (.e200 MVU), OR
maximum • .e6 hours with inadequate uterine contractions despite oxytocin
slope • Arrest disorder as indication for CS will only apply at this phase
Pelvic Division JI
Prolonged deceleration phase:
• Nullipara: ;,3 hours
• Multipara: .el hour

Deceleration Secondary to•:

8-9cm
phase • Failure of descent due to contracted pelvic inlet: fetal head remained
at station "O" or above (-1 to -5) for .el hour. Delivery by CS
• Arrest of descent due to contracted pelvic midplane: fetal head
remained at a station from +1 to +5 for .el hour (e.g., station +1 for
;el hour). Delivery by CS
Prolonged second stage
• Nu1lipara: 2 hours or 3 hours (if with epidural)
• Multipara: 1 hour or 2 hours (if with epidural)

Secondary to••:
10cm Second
• Failure of descent due to contracted pelvic inlet: fetal head only at
(fully) Stage
station "O" or above (-1 to -5) for >l hour. Delivery by CS
• Arrest of descent due to contracted pelvic mid plane: fetal head at
station + 1 to +5 for> 1 hour. Delivery by CS
• If fetal scalp is already seen separating the labia (station +5) & fetal
head is in occiput anterior, outlet forceps delivery can be attempted
'Must meetcriteriaof prolonged
decelerationphase beforeaddingseconda,ydiagnosisofeither'failure"or "arrest ofdescent'
"Must meet criteriaof prolonged2nd stage beforeaddingthe seconda,y diagnosisof either'failure"or "arrestof descent'
Source: PhilippineObstetrical& GynecologicalSociety;2021
124
 Guide to use the table from the previous page:
• Perform internal exam to determine cervical dilatation, station, and Bishop Score
• Check the indication for induction of labor
• Patient meets the criteria ofadequate labor (contractions with ;,200 MVUat least every 2-3 minutes)
• Check the phase of labor the patient is in
• Check if the patient's labor pattern fits the criteria for abnormal labor
Some Sample Cases
1. Failed induction of labor: GlPO 39 weeks AOG with GDM for induction of labor.
Internal examination (IE) was 2 cm, 50%, station -3, (+)bag of waters (BOW); with
no perceived uterine contractions. Induction with oxytocin drip started which made
uterine contractions regular with ;,ZOO MVU intensity. Amniotomy was done to further
1.·
augment labor. Twelve (12) hours from complete induction (oxytocin drip, ruptured
BOW, and regular contractions of ;,ZOOMVU), the cervix remained in the latent phase.
2. Active phase arrest or arrest of cervical dilatation: GlPO 39 weeks AOG with
ruptured bag of waters on admission. IE revealed: 6 cm, 70% station -1, (-) BOW with
clear fluid. Augmentation of labor with oxytocin was done. After 4 hours with regular
strong uterine contraction, IE remains unchanged at 6cm, 70%, station -1.
3. Prolonged deceleration phase secondary to failure of descent secondary to
contracted pelvic inlet: GlPO 39 weeks AOG came in due to watery vaginal discharge.
Augmentation of labor with oxytocin was started with normal progress of labor until
IE was 8 cm, 80%, station -1, (-) BOW. For 4 hours, it remained the same. This is
prolonged deceleration phase secondary to failure of descent since the fetal head did
not descend below station 0.
4. Prolonged second stage secondary to arrest of descent secondary to contracted
pelvic midplane: GlPO 39 weeks AOG came in due to watery vaginal discharge.
Augmentation of labor with oxytocin was started with normal progress of labor until
IE was 8 cm, 80%, station +1, (-)BOW.For 3 hours, it remained the same. This is
prolonged 2nd stage secondary to arrest of descent since the fetal head remained in
that same station for> 1 hour.
Sources:WilliamsObstetrics,25th Edition,2018;PhilippineObstetrical& Gynecological
Society
PracticeBulletinNumber2, April5, 2021;Cohen,et al. UniversityPark Press; 1983
II. ABNORMALLABORPATTERNS,DIAGNOSTICCRITERIA,AND TREATMENT
CRITERIA
LABOR PATTERN TREATMENT

Prolongation Disor.der
I NuIiiparas I Multiparas I
• Bed rest*
Prolonged latent phase >20 hours >14 hours • Oxytocin or CS for
urgent problems
Protracition Disorders
Protracted active-phase dilation <1.2 cm/hr <1.5 cm/hr • Expectant & support*
Protracted descent <l cm/hr <2 cm/hr • CSfor CPD

Arrest Disord·ers
-
Prolonged deceleration phase >3 hours >1 hour
Secondary arrest of dilation
>2 hours >2 hours • CSif with CPD*
(arrest of cervical dilatation)
• Oxytocin if no CPD*
Arrest of descent >l hour >l hour • Rest if exhausted
No descent in deceleration phase
Failure of descent
or second stage
>3 hours:(+) RA >2 hours:(+) RA • Forceps or vacuum*
Prolonged second stage • cs
>2 hours:(-) RA >l hour:(-) RA
•Preferredtreatment
125
"POWER"
• Cervical dilation & propulsion and expulsion of the fetus are brought about by
contractions of the uterus
• During second-stage labo,; uterine contractions are also reinforced by "pushing" of the
mother (voluntary or involuntary muscular action of the abdominal wall)
• Either of these factors may lack intensity & result in delayed or interrupted labor:
0 Uterine Contractility
0 Expulsive Powers

I. PHYSIOLOGYOF UTERINECONTRACTION
• A uterus with a good power should have a fundal dominance: uterine fundus contracts
effectively pushing the fetus towards the birth canal & retracting the cervix to fully dilate
• Power is defined as uterine contractility multiplied by the frequency of contractions

210 -r- 7--,, TT'7TTT -- --i-TT - - rTTTTTTIT IT rr,17

I
I I 11
10 min

I
-1-tH+-
i . I I I 1J

+t
11

I 11
\--- --t+

Montevideo Units (MVU):

• Calculated by subtracting the baseline uterine pressure from the peak contraction
pressure for each contraction in a 10-minute window and adding the pressures
generated by each contraction
• Adequate contractions: 2'200 Montevideo units (MVU)per 10 minutes for 2 hours
• In the example above, there are five contractions, producing pressure changes of
52, 50, 47, 44, and 49 mmHg (respectively). The sum of these five contractions is
242 Montevideo units

126
II. UTERINE DYSFUNCTION
• As labor normally progresses, there is an increase in intensity, duration, & frequency of
uterine contraction (i.e., uterine contraction increases from latent phase to the active phase)
• Failure of the cervix to dilate or the presenting part to descend is cause for concern

PARAMETERS
I HYPOTONIC UTERINE
DYSFUNCTION
I HYPERTONIC UTERINE
DYSFUNCTION
Low uterine activity (hypotonic) I High uterine activity (hypertonic)
Ettopathogenesis
- -··

General
features
• Absence of basal hypertonus
• Normal gradient pattern with
fundal dominance
• Elevated basal tone (basal
hypertonus) due to absence of
fundal dominance, and/or
• Complete asynchronism of the
I
impulses originating in each cornu
• Gradient pattern is distorted
(e.g., incoordinate uterine
dysfunction)
• The slight rise in pressure during
• Uterine pain that appears out
Pathology contraction is insufficient to
of proportion to the intensity
dilate the cervix
of the contractions and their
effectiveness in effacing and
dilating the cervix
Prevalence • More common • Less common
• Uterine overdistention (e.g.,
• Contraction of the midsegment
macrosomia, polyhydramnios)
of the uterus
Etiology • Grand multiparity
• Asynchronism of the impulses
• Sedation
originating from each cornu
• Regional anesthesia
Manifestations and Diggnosis ;
'
Clinical
• Painless • Painful
symptoms
Fetal distress • Late • Early
,,,~
Management i ' ~

• Discontinue oxytocin to allow the

• Acts promptly, leading to
uterus to rest or reboot
Oxytocin noticeable progress
• Cesarean delivery for the usual
• CPD must be ruled out first*
obstetrical indications
Value of
• Not useful • Useful
sedation
'Normalclinicalpelvimetryor adequate pelvis:
Normaldiagonalconjugate
Pelvicsidewallsnearlyparallel
lschialspines not prominent
Sacrumhollow
Subpubicangle not narrow
Occiputis the presentingpart
Fetal head is engaged

Ifthese are present, most likelycause of dystociais uterinedysfunction

127
III. OTHER POWER ABNORMALITIES FROM LABOR DISORDERS
A. Maternal Pushing Efforts
° Combined force created by contractions of the uterus and abdominal musculature
propels the fetus downward.
° Factors that affect maternal pushing:
• Heavy sedation or regional anesthesia reduce the reflex urge to push
• Intense pain created by bearing down overrides urge to push
0 Approaches to improve pushing with epidural anesthesia:
• Pushing forcefully with contractions after complete dilation, regardless of the urge
to push
• Analgesia infusion is stopped and pushing begins only after the woman regains the
sensory urge to bear down

B. Other Risks for Uterine Dysfunction

0 Neuraxial analgesia can slow labor and has been associated with lengthening both first
and second stages of labor and slowing the rate of fetal descent
° Chorioamnionitis is associated with prolonged labor, and this maternal intrapartum
infection itself contributes to abnormal uterine activity
0 Uterine infection is a consequence of dysfunctional, prolonged labor rather than a
cause of dystocia
"PASSENGER" (FETUS)
• Normally, the fetus is in a cephalic vertex presentation and in the occiput anterior (OA)
position, for a successful vaginal delivery
• Abnormalities can occur in the following: position, presentation, size, or development
• May be due to:
0 Malpositions
0 Malpresentations
0 Excessive fetal size

I NORMAL
I ABNORMALITIES

• Malposition
Position • Occiput anterior (OA) Persistent occiput transverse (OT) position
0

Persistent occiput posterior (OP) position

0

• Malpresentation
• Vertex cephalic Brow /face presentation
0
Presentation
presentation Breech presentation
0

Transverse presentation
0

I. BROW PRESENTATION
• Cephalic presentation wherein the head is "partially extended" (usually converts to a face
or occiput presentation)
• Rare presentation when the portion of the fetal head between the orbital ridge and
anterior fontanel presents at the pelvic inlet
• Fetal head occupies a position midway between full flexion (occiput) and extension (face)

• Presenting diameter is occipitomental

(12.5 cm), which is the longest diameter
(therefore, vaginal delivery is not possible)
• More than half of the fetal head is above the
symphysis pubis
• Occiput (triangle-shaped posterior fontanel)
is palpable at a higher level than the sinciput
(diamond-shaped anterior fontanel or
bregma)
• The following can be felt on vaginal exam:
0 Anterior fontanel, frontal sutures
0 Orbital ridges, eyes
0 Root of nose

128
 B. Management
0 A larger diameter must pass through the pelvis
0 Iffetus is extremely small (e.g.,preterm) or pelvis is particularly large, the brow presentation
may convert to vertex or face presentation (mentum anterior) to deliver vaginally

• Engagement of the fetal head and subsequent delivery cannot

take place as long as the brow presentation persists (because of
lack of engagement and arrested labor]
Trial of labor &
• Vaginal delivery is considered if:
vaginal delivery
° Fetus is small and the pelvis is large

Cesarean section
0 Spontaneous conversion into an occiput or face (mentum
anterior] presentation
• Done in cases of persistent brow presentation
I
II. FACEPRESENTATION
• In this presentation, the fetal head is fully extended (hyperextended)
• The occiput is in contact with the fetal back and the chin (mentum) is presenting
• Fetal face may present with mentum anterior or posterior

A. Etiopathogenesis
0Preterm fetus (a smaller head can engage before conversion to vertex position]
0Marked enlargement of the neck or coils of cord around the neck may cause extension.
° Fetal malformations and hydramnios are risk factors for face or brow presentations
0Anencephalic fetuses naturally present by the face
° Contracted pelvis or a large fetus
0High parity (a pendulous abdomen permits the back of the fetus to sag forward or
laterally, often in the same direction in which the occiput points which promotes
extension of the cervical and thoracic spine)

B. Diagnosis

• Presenting diameter is the

submentobregmatic (9.5 cm]
• Groove may be felt between the occiput
and the back (because of the extended
head)
• Distinctive facial features are palpated:
mouth, nose, malar bones and orbital
ridges
• Occiput or sinciput are not palpated on
vaginal examination

C. Management
0 Mentum anterior: the only face presentation that will allow for a vaginal delivery,
since symphysis pubis serves as a fulcrum allowing for flexion of the hyperextended head
0 Mentum posterior or transverse: CS is necessary because fetal brow (bregma) is
pressed against the maternal symphysis pubis (not amenable to vaginal delivery)
0 Mentum posterior:
• Spontaneous rotation to mentum anterior may occur in some multiparous patients
with an adequate pelvis & smaller fetus compared to previous babies. Trial of labor can
be attempted with a low threshold for CS
• In multiparous patients with previous babies smaller than current one or in
nulliparous patients, CS may be done early in the course of labor

129
III. BREECHPRESENTATION
• Occurs when the breech (fetal buttocks) or lower extremities present into the maternal pelvis
• Types of breech (e.g., frank complete, incomplete) discussed in previous chapter

A. Etiopathogenesis
RISK FACTORS FOR
BREECH PRESENTATION
I COMPLICATIONS OF
BREECH PRESENTATION
• Prematurity (20-30%)
• Perinatal morbidity /mortality (e.g.,
• Uterine relaxation (multiparity)
preterm delivery, birth trauma, congenital
• Multiple pregnancy
anomalies)
• Hydramnios, oligohydramnios
• Low birth weight (prematurity, lUGR)
• Hydrocephalus
• Prolapsed cord
• Anencephaly
• Placenta previa
• Uterine anomalies/tumor
• Uterine anomalies/tumors
• Placenta previa

B. Diagnosis of Breech Presentation

1. Vaginal Examination
INCOMPLETE/

I FRANK BREECH
PRESENTATION
I COMPLETE
BREECH
PRESENTATION
I FOOTLING
BREECH
PRESENTATION

Illustration
(-j-,
~...
.'->\
.
/ ,;
_.,,
(~-,
'\ 1

"\.~ \~·,
/

'?'~
/_./
~
(?/
>~_,,.---'-....
~:::--_c~) '<·/-,<:_,,.. )

• One or both hips

• Lower extremities
are not flexed
are flexed at the
• One or both knees • One or both feet
hips & extended at
are flexed or knees lie below
Description the knees
• Both legs are the breech, such
• The feet lie in close
flexed at the hips that a foot or knee
proximity to the
is lowermost in the
head
birth canal
• Palpable fetal
• lschial
buttocks, anus, • One foot or both
Vaginal Tuberosities
sacrum, ischial feet
examination • Sacrum
tuberosities • Sacrum cannot be
findings • Anus
• Feet cannot be palpated
• External Genitalia
palpated

130
 2. Leopold Maneuvers
LM 1 I LM 2 I LM 3 I LM 4

. . .
. - =-- t -

) • ) ) >

1---- ___ 1_)__ - ---II

• Fetal back on • (Unengaged)
• Hard, round, • (Engaged) firm
one side of the breech is
ballotable fetal breech beneath
abdomen & small movable above
head symphysis pubis
parts on the other pelvic inlet

3. Others Ways to Diagnose Breech Presentation

• Location of fetal heart tones (FHT)
• Radiography: to determine if the head is extended (fetal head extension)
• Ultrasonography: to identify fetal anomalies

C. Management of Breech
0 Planned vaginal versus planned CS for term, singleton delivery
0 External version may be attempted (repositioning the breech baby)

1. Vaginal Delivery may be attempted for the following:

• Frank or complete breech presentation
• Partial breech extraction (PBE), or
• Complete (total) breech extraction

2. Cesarean Section is indicated for the following:

MATERNAL FACTORS I FETAL FACTORS
• Pelvis is contracted or has an • Large fetus
unfavorable shape • Hyperextended head (""stargazing breech")
• Delivery is indicated (i.e., patient not • Incomplete/ footling breech
in labor) • Healthy preterm fetus where delivery is
• Uterine dysfunction indicated
• Lack of experienced operator for • Severe IUGR
vaginal breech delivery • Previous perinatal death/ birth trauma

131
IV.TRANSVERSEPRESENTATION
• This position occurs when the long axis of the fetus is perpendicular to that of the mother
• There is no mechanism of labor for transverse lie
• Always delivered by cesarean section
A. Etiology
0Abdominal wall relaxation
0Preterm fetus
0Placenta previa
0Abnormal uterine anatomy (e.g., multiple myoma, especially if occupying the lower
uterine segment)
, Polyhydramnios
'Contracted pelvis
B. Diagnosis
1. Abdominal and Vaginal Examination

Abdominal • The abdomen is usually wide

examination • Uterine fund us extends to only slightly above the umbilicus
Vaginal • Palpation of the acromion and hands
examination • "Gridiron": we can feel the ribs ("feel of the ribs")

2. Leopold Maneuver

• Position of back is readily identifiable

• No fetal pole is detected in the fund us • When back is anterior, a hard resistance
• The ballotable head is found in one iliac plane extends across front of abdomen
Fossa and the breech in the other • When back is posterior, irregular nodules
(small parts) are felt in abdominal wall

V. EXCESSIVEFETALBODYAND HEADSIZE
• Fetal size alone is seldom suitable explanation for failed labor
• There is no current method of measurement satisfactorily predicts fetopelvic
disproportion based on head size
ABNORMALITY REMARKS
• Definition: birth weight ~4,000 grams irrespective of AOGor
>90th percentile for gestational age after correcting for neonatal sex
Fetal
& ethnicity
Macrosomia
• Total length of labor is not prolonged - but the second stage of labor is
prolonged
• Excessive accumulation of cerebrospinal fluid (CSF)with consequent
cranial enlargement
Hydrocephalus
• Gross cephalopelvic disproportion is the rule, with dystocia as the
usual consequence

132
"PASSAGE" (PELVIS OF MOTHER)
• Fetopelvic disproportion arises from diminished pelvic capacity, excessive fetal size, or both
• Any contraction of the pelvic diameter that diminishes the pelvic capacity can create
dystocia during labor
• Pelvic contraction is discussed below

The Inlet
t--P_e_lv_i_c_b_r_im_(_fo_r_e_p_e_lv_i_s_)-+-_•_R_o_u_n_d
Diagonal conjugate
____________________
• e,11.5 cm
----t I
The Midpelvis
Symphysis pubis • Parallel to the sacrum and with average thickness
Sacrum • Hollow with average inclination
Side walls • Non-convergent
lschial spines • Blunt
Interspinous diameter • e,10 cm
Sacrosciatic notch • Sacrospinous ligament is 2.5-3 fingerbreadths
The Outlet
Suprapubic angle • Admits 2 fingerbreadths
Coccyx • Mobile
Anteroposterior
• e,11 cm (from tip of sacrum to inferior edge of symphysis)
diameter
Clinicalpelvimetryfindingsof a contracted
pelvis:
• Diagonal conjugate<11.5cm • Prominentischialspines
• Pelvicsidewallsareconvergent • Subpubic
archangle<90degrees
• Sacrumis flat • Nodescentof vertexwithValsalvaor fundalpressure
(Muller-Hiilis
maneuver)
Overview of Pelvic Contraction

LJJUUJ:Si
rtr
PELVIC INLET MIDPLANE PELVIC OUTLET

'
CONTRACTION CONTRACTION CONTRACTION
• Causes transverse • Defined as an
arrest of fetal head interischiat tuberous
General • Shortest AP diameter is
• Spines are sharp & diameter of <8 cm,
description <10 cm
prominent sidewalls roughly measured
or clinical long or if its greatest
are convergent using the length of a
pelvimetry transverse diameter
• Narrow sacrosciatic closed fist against the
findings <12 cm
notch perineum
• Flat sacrum • Narrow pubic arch
• Obstetrical conjugate
• Often associated
(AP diameter) <10 cm • Interspinous
Measurement with a contracted
• Transverse diameter diameter <8 cm
midplane
<12 cm
• Frequently causes
• More frequent face and transverse arrest of • May play an
shoulder presentations the fetal head, which important part
Effects
• More frequent cord can lead to difficult in production of
prolapse midforceps operation perinea! tears
or cesarean delivery
Sources:WilliamsObstetrics,
25thEdition,2018;DrennanK, 2021.
133
REFERENCES
I.CohenW, FriedmanEA:Managementof Labor.Baltimore,UniversityPark Press,1983
2.CohenWR. Friedman EA Perilsof the new labor managementguidelines.Am J ObstetGynecol2015; 212:420.
3.Cunningham, F.G., Leveno, K. J., Bloom, S. L.,Spong, C. Y.,Dashe, ). S., Hoffman, B. L.,Sheffield,). S. (2018). Williams Obstetrics
(25th edition.).New York:McGraw-HillEducation.
4.Drennan K. Abnormal labor: diagnosis and management I GLOWM [Internet]. [cited 2021 Oct 7). Available from: http://
www.glowm.com/section-view /heading/abnormal-labor-diagnosis-and-rnanagement/item/13 2
5.Ehsanipoor RM, Satin AJ.Normal and abnormal labor progression. Uptodate. Available online: https://www.uptodate.com/
contents/normal-and-abnonnal-labor-progression?. Accessed on Sept 21, 2021
6.EI-Movafi DM. Obstetrics simplified: Contracted pelvis. Available onlinehttps://www.gfmer.ch/ Obstetrics_simplified/.
Availableonline Sept 21, 2021
?.FriedmanE.The graphicanalysisof labor.Am J ObstetGynecol1954; 68:1568.
8.Friedman EA.Labor:ClinicalEvaluationand Management.2nd ed, Appleton-Century-Crofts, New York 1978.
9.Myles TD, SantolayaJ.Maternal and neonatal outcomesin patients with a prolongedsecondstageof labor.ObstetGynecol
2003; 102:52.
10. PhilippineObstetrical& Gynecological SocietyPracticeBulletin Number 2, April 5, 2021
11. Zhang I, Duan T.The physiologic pattern of normal labour progression. BJOG2018; 125:955.
12. Zhang I, Troendle J, Mikolajczyk R, eta!. The nan,ral histo,y of the normal firststageoflabor. ObstetGynecol 2010; 115:705.

134
PROCEDURES
INOBSTETRICS
 SECTION ONE
INSTRUMEN:rS USED IN OBSTETRICS AND GYNECOLOGY

GENERAL SURGICAL INSTRUMENTATION

• Knowledge in the use of needles, sutures, & instruments is the foundation of any surgeon
• There are distinct advantages/disadvantages for each instrument in certain situations

I. SURGICALSUTURES
• Used to ligate bleeding vessels or approximate tissue

• PolyglycolicAcid
• Polyglactin 910
I
• Lactomer 9-1, and
Glycomer 631
• Nylon
• Plain • Polyglyconate and • Surgical silk or
• Polyester
• Chromic Catgut Polydioxanone cotton
• Polypropylene
• Poliglecaprone 25
• Polyglactin 910
(Rapide)
• Polyglytone 6211

II. SURGICALNEEDLES
• Characteristics of needles include their attachment to the suture, shape of the tip, suture
lever in tissue, and the curve of the needle
• Necessary to carry suture material through tissue
•Needlepoint (or sharp apex): sharpness
and geometry are critically important
characteristics
Needle point\ • Body: portion of the needle which is
Needle eye
grasped by the needle holder
l'-''lr-•Needle diameter • Needle length: the circumferential length
of the needle
• Needle cord length: linear distance between
the pointed tip & the end of the needle
• Eye: opening where to manually insert
non-atraumatic sutures (Note: atraumatic
sutures have eyeless needles with the
Needle length suture already permanently attached into
a hollow end which is less traumatic to the
tissues, hence the name)

137
III. NEEDLEHOLDERS
• Required when curved needles are used
• With broad tips having a variety of inner surfaces to prevent needle from slipping/rotating
WAGENSTEEN (STRAIGHT) I HEANEY (ANGLED)

• Can place sutures deep inside the pelvis • Useful for vaginal surgeries since angled
head allows easy placement of curved
needles & sutures at any angle

-+ ¥ :-4

IV.SCALPEL
• Best instrument for dividing tissue with minimal trauma to surrounding tissue
• Scalpel blades come in various sizes and shapes depending on the cutting task at hand
Function follows form when it comes to surgical blades
0 In general: larger blades are used for coarser tissues or larger incisions

A. Scalpels
SIZE 10 I SIZE 11 I SIZE 15 I SIZE 20 I SIZE 22

• Large curved • Long, • Small, curbed • Long edge is • Larger

cutting edge triangular cutting edge ideal in initial version of
• Most versatile blade with • Used for finer skin incisions size 10
• Used for sharpest incisions for quickly • Flat,
cutting large edge at the covering unsharpened
incisions hypotenuse distance back edge
across soft • For stabbing • Used for cutting and short
tissues incision and/ tissue & curved
• Held at 20-30 or short precise procedures cutting edge
degree angle shallow cuts that require • Use to create
to the skin • Can incise large incision
puncturing
with minimal
through • Also held at usually
wrist/finger
tough-walled 20-30° angle through thick
movement
abscesses for to the skin skin
drainage (e.g., with minimal
Bartholin wrist/finger
gland duct) movement

~
/,,
/
/

Source:Yeomans
ER.et al. Cunningham
andGilstrap'sOperative
Obstetrics
(3rdEd);2017

138
 B. Two Methods for Gripping

"PENCIL-GRIP"/ "PRECISION GRIP" I "POWER ~,: 1;,:;: ~~',~!;IN GRIP"/

• Scalpel is held as one would a pencil, and
movement is directed by the thumb and
index finger
• Motion comes predominantly from the
thumb & index finger, allowing for precise
cutting of tissue
• Scalpel is held between the thumb and
third finger
• The end of the blade is forced up against
the thenar muscles of the hand
• Primarily used for making long skin
incisions, using arm motion, rather than
finger motion

I
Source:YeomansER,et al. Cunningham
andGilstrap'sOperativeObstetrics(3rdEd);2017

V. SCISSORS
• For cutting and for blunt dissection
• May be:
Straight: designed for cutting body tissues near the surface of a wound
° Curved: cut tissue in a smooth curve & horizontal fashion, cutting deep into a wound

MAYO I METZENBAUM I IRIS I SUTURE

SCISSORS

• Used when • For retro peritoneal • For delicate • With a blunt and
dividing tough dissection or for dissection a hooked tip for
tissue (e.g., fascia, developing tissue suture removal
parametrial tissue planes in adhered (not used on
of vaginal cuff) or distorted tissue tissue)

139
VI. TISSUE/THUMB FORCEPS
• Consists of two strips of metal joined at one end
• Used to grasp and hold tissue during dissection, suturing, or cutting
RING- BONNEY
SMOOTH DEBAKEY TOOTHED ADSON
TIPPED TISSUE
FORCEPS
I FORCEPS
I FORCEPS
I FORCEPS
I FORCEPS
I FORCEPS
• For • Have long • Bites into • Have fine • Increase • Heavy-
handling fine smooth tissue, teeth the toothed
friable or tips that providing and are grasping forcepswith
delicate provide a firm commonly force serrations
tissue precise grip with used to without along the
control of minimal approximate using teeth shaft for
small or pressure skin for when a maximum
delicate staple or secure gripping
tissue (e.g., suture hold is powerused
vascular placement needed whensewing

i
.
surgery)

I :
fascia

' fflfl R /ilA 7":'=: ,

I
it
i ~ -- ~ ~t
-- ~
;; ~ "" -:.~
;< ~
<
,,
' § 1/
~-
...
I!
~ I\
~

-
VII. CLAMPS/GRASPINGFORCEPS
To grasp and apply pressure or traction to tissues
• With finger rings and locking mechanism

BABCOCK I ALLIS I KOCHER/

OCHSNER
I RING FORCEPS

• No teeth • With serrated • Have transverse • Commonly used

[atraumatic] to edges with short ridges along shaft to hold folded
hold delicate teeth & interlocking sponges
tissues teeth at the tip
to grasp heavy
tissues

140
 HEANEY I HEANEY- BALLENTINE I MASTERSON

• Heavy hysterectomy clamps with ridged shaft for clamping the parametrial and
paracervical tissue during hysterectomy

I
.

VIII. RETRACTORS
• Instrument to separate edges of a surgical incision/wound, or to hold back underlying
organs/tissues so that body parts within the incision may be accessed (to improve
exposure)
A. Self-Retaining Retractors: to hold incision apart

BOOKWALTER I BALFOUR

• Consists of a circular metal ring to which a wide • Two lateral blade with one additional
variety of retractors can be attached at any point retractor blade

O'CONNER-0-SULLIVAN

• Circular retractor with four blades

141
B. Manual Retractors
HEANEY
• Offers reliable atraumatic
traction on delicate
tissues (e.g., urinary
bladder and peritoneum)
• Used in gynecologic
surgeries ( e.g., vaginal
hysterectomy)
BRIESKY-NAVRATIL
VAGINAL SPECULUM
• Special curved jaws help
visualize the genital tract
• For opening the vagina
and visualization of
cervix, vaginal walls and
uterine cavity
• For pap smear and other
gyne procedures
Source:YeomansER,et al. Cunninghamand Gilstrap'sOperativeObstetrics(3rdEd);2017
I DEAVER
• Shaped like a question
mark
• Helps widen surgical
incisions and hold large
abdominal cavity organs
• Hook used to rest on
surgeon's fingers
I ARMY-NAVY
• For retraction of shallow
or superficial incisions
142
I RICHARDSON
• Crescent-shaped with
ergonomic hollow handle
• For atraumatic blade
insertion and deep
traction
I PARKER
• Two concave blades with
double ended design and
central handle
• For strong tractions to
widen surgical field or
pull back soft tissues
DILATORS AND CURETTES FOR DILATION & CURETTAGE
• Dilation and curettage (D&C) is a procedure in which the physician explores a cavity
beyond his/her view
• "Dilation" refers to the opening of the cervix
• "Curettage" refers to the removal of tissue within the uterus with an instrument called a curette

I. DILATORS
• Metal or plastic cylindrical rods of increasing diameter used to dilate the cervical os to
sufficient size to admit other surgical instruments into the uterine cavity
• Dilation of the internal os should be done slowly, allowing the fibers of the internal os to
stretch gradually
HANK I PRATT I HE GAR

• Tapered tips that reach
deep into the cervix
• Cause cervical relaxation
and uterine dilation
• Smooth edges allow
comfortable insertion with
minimal damage and less
chance of piercing
• Long tapered tips that
enables easier dilation
• Less traumatic but may
perforate smaller uterus
■
• Rounded tip (short)
• For small or atrophic
uterus
• Usually a set of dilators of
increasing caliber

II. CURETTES (FOR ENDOCERVICALCURETTESTAGE)

• In postmenopausal bleeding or suspected malignancy, the endocervical canal should be
curetted before cervical dilation
KEVORKIAN I SIMS I THOMAS

• Narrow, boxlike cutting • Small (3 mm), medium • Dull serrated blade

edge (6 mm) and large (16 mm) • For exploration of the soft
• Medium curette is adequate uterus of an early abortion
for most diagnostic D&C's
• Large curette is for
incomplete late abortions
& postpartum bleeding

,=,o

I J

:
I I I

Source:Yeomans
ER,et al. Cunningham
andGilstraps Operative
Obstetncs(3rdEd),2017
Hulka,J, Glob.libr.women'smed;2008
143
 SECTION TWO
OPERATIVE VAGINAL DELIVERY

OVERVIEW OF OPERATIVE VAGINAL DELIVERY

• Refers to a delivery in which the operator uses forceps, a vacuum, or other devices to
extract the fetus from the vagina, with or without the assistance of maternal pushing
Most important function of forceps/vacuum device: traction
Additional function of forceps: rotation of the fetal head (e.g., in occiput transverse and
posterior positions)

I. INDICATIONS:
• Termination of 2nd stage of labor indicated in conditions where threat to mother/fetus is
relieved by delivery. The following must be observed:
Must be non-elective
0 Should fulfill the criteria for an outlet forceps delivery

FETAL INDICATIONS I MATERNAL INDICATIONS

• Prolonged 2nd stage of labor (most common)*

• Non-reassuring fetal heart rate pattern • Heart disease
• Premature placental separation • Pulmonary injury or compromise
• Suspicion of immediate or potential • lntrapartum infection
fetal compromise • Neurological conditions
• Maternal exhaustion; inability to push effectively
'Definitionof ProlongedSecondStageof Labor:
0 Nulliparous:lackof progress>3 hoursif withregionalanesthesia
(>2hoursif withoutregionalanesthesia)
0 Multiparous: lackof progress>2 hoursif withregionalanesthesia
(>1hourif withoutregionalanesthesia)
Source:ACOG.ObstetGynecol;2020

II. RISK DISCRIMINATORSFOR OPERATIVEVAGINALDELIVERY

• Deliveries categorized as outlet, low or mid pelvic procedures (high forceps not done in
contemporary obstetrics)
• Two most important discriminators of risk for mother and infant:
0Station
0Rotation

STATION I ROTATION

• Fetal station is measured using the -5 to +S • The distance of the clockwise

centimeter classification system or counterclockwise motion
• Safety of forceps is directly proportional to the needed for the occiput (posterior
station of the fetal head fontanel) to move towards the
• The higher the station = the greater the risk symphysis pubis

144
III. PREREQUISITES FOR OPERATIVE VAGINALDELIVERY
Mnemonic: "FORCEPS":
• Fully dilated cervix, no fetal coagulopathy or fetal demineralization disorder
• Occiput/vertex presentation
• Ruptured membranes
• Cephalopelvic disproportion is not suspected, Consent completed
• Engaged head (at least +4 station), experienced operator, emptied maternal bladder
• Position of fetal head is known, painless (adequate anesthesia)
• Size (fetal weight) estimated

IV. CONTRAINDICATIONSTO INSTRUMENTALDELIVERY

• If risk to mother or fetus is deemed unacceptable
• Extreme fetal prematurity

■
• Fetal demineralizing disease (e.g., osteogenesis imperfecta)
• Fetal bleeding diathesis (e.g., fetal hemophilia)
• Unengaged head (i.e., head is engaged when biparietal diameter has reached pelvic inlet) ..
• Fetal position: unknown or in brow /face position
• Suspected fetal-pelvic disproportion
Source:AGOG.ObstelGynecol;2020

FORCEPS DELIVERY
• Elective forceps delivery should be done only when criteria for outlet forceps have been met
• Forceps is usually called the "Iron Hand" (designed for extraction of the fetus)

I. PARTS OF THE FORCEPS

BRANCH
I REMARKS
• Parts: toe, heel and two (2) curves
Blade Outward cephalic curve: conforms to the round fetal head
0

Upward pelvic curve: corresponds to the axis of the birth canal

0

Shank • Parallel or overlapping

• Connect the right and left branches and stabilize the instrument
• Types:
Locks English lock: end of the shank
0

Pivot lock: end of the handles

0

Sliding lock: along the shank

0

II. CLASSIFICATION/CRITERIAFOR FORCEPSDELIVERY

• Based on station and extent of rotation (these factors correlate with the level of difficulty
and procedure-related risk)
• Note that a lower fetal station and smaller degree of head rotation are associated with
less risk for injury
• Outlet forceps, midforceps or low forceps delivery describes the level or position of the
fetal presenting part where the forceps is applied
PROCEDURE I CRITERIA FOR ELECTIVE FORCEPS DELIVERY
• Scalp is visible at the introitus without separating the labia
• Fetal skull has reached the pelvic floor
Outlet
• Fetal head is at or on the perineum
forceps
• Head is occiput anterior (OA) or occiput posterior (OP), or
• Head is right or left OA or OP position but rotation <45 degrees
• Leading point of fetal skull is at station 2:+2 cm, and not on the pelvic
Low forceps floor, and (two categories):
(two types) 0 Rotation is <45 degrees, or

0 Rotation is >45 degrees

Mid forceps • Station is between O and +2 cm

Source:CunninghamFG,et al. Williams
obstetrics;2018;AGOG.ObstetGynecol;2020
145
III.TYPES OF FORCEPS
TYPE I REMARKS I ILLUSTRATION
• Fenestrated blades, parallel
shanks and English lock
Simpson • Best fit for a molded head:
(most the elongated cephalic curve
common) accommodates the fetal head
• Usedto deliver fetus with a molded Cephalic curve
head, common in nullipara

TBr T
• Thin smooth blades Handle Lock

• Better for fetus with rounded,

Tucker
unmolded head (common in
Shank
Mclane
multipara) because the cephalic
curve of forceps in more concave Pefv,ccu,vey
• Used for delivery of the Hanl
die Lolck==='=h•=n;;;k
;;;;;H,.;:~1·'
Bt• Tri
aftercoming head in breech

~~
Piper
• Shanks are long
• It has a reverse pelvic curve
Cephalic curve

• Best used for midforceps delivery

"TeLr T Br• T
~
Kielland • Good for correction of transverse
arrest & pelvic rotations Shank,
Cephalic curve

IV. FORCEPSPROCEDURE
Ask for
• Authorization (consent), Anesthesia, Assistance
Assistance
Bladder • Empty bladder
Cervix • Fully dilated; membranes ruptured
Determine • Station, position, adequate pelvis, shoulder dystocia
Equipment • Quality, functionality
• Phantom application; correct pair
• Left blade, left hand, maternal left side
• Pencil grip, vertical insertion, left thumb directing
• Right blade, Right hand, maternal right side
Forceps
• Pencil grip, vertical insertion, right thumb directing
• Lock & support
• Posterior fontanelle 1 cm above plane of shank
• Sagittal suture perpendicular to plane of shank
Gentle
• Traction with contraction or pushing
traction

Handle • Traction along axis of canal

elevation • Do not elevate too early
Incision • Episiotomy (if applicable)
• Remove forceps when fetal jaw is visible
Jaw • Inspect for perinea! and cervical lacerations
• Document
Source:ALARM.Societyof Obstetricians
andGynecelogists
of Canada;2012-2013
146
V. STEPS FOR FORCEPSBLADEAPPLICATIONAND DELIVERY(OCCIPUTANTERIOR)

STEPS I ILLUSTRATION

• Two or more fingers of the right

hand are introduced inside the left
portion of the vulva and then into
~
the vagina beside the fetal head

• Handle of the left branch is grasped

between the thumb and 2 fingers of
the left hand (pencil grip)

• Blade tip is gently passed into the

vagina between the fetal head and
the palmar surface of the fingers of
4 I
the right hand. Same is done for the
right branch using the opposite hand

• After positioning, the branches are

articulated

• Fetal head is perfectly grasped only

Posterior
when the long axis of the blades fontanelle
corresponds to the occipitomental
diameter Flexion
point
• Appropriately applied blades are
equidistant from the sagittal suture
Anterior
fontanelle
• Each blade is equidistant from its ~<~~"'1'--
adjacent lambdoidal suture

• Rotation to occiput anterior is

performed before traction is applied

• When blades are placed

satisfactorily, then gently,
intermittent, horizontal traction is
exerted concurrent with maternal
efforts until the perineum begins
to bulge

• With traction, as the vulva is

distended by the occiput, an
episiotomy may be performed if
indicated
• Handles gradually elevated,
eventually pointing almost directly
upward as the parietal bone emerge.
The head is extended
• Forceps may be removed
• Spontaneous delivery should follow
with maternal pushing

147
VI. FAILEDFORCEPS
• If satisfactory application of forceps cannot be achieved, abandon procedure and deliver
either by vacuum extraction or CS
• If after 3 gentle downward pulls do not result in descent, abandon the procedure and
deliver by CS
• Factors for failed forceps-assisted delivery:
0 Persistent occiput posterior
0 Absence of regional or general anesthesia
0 Birthweight >4 kg
Source:AGOG,2012

VII. MORBIDITY& COMPLICATIONS

MATERNAL MORBIDITY I PERINATAL MORBIDITY

• Lacerations: 3rd & 4th degree lacerations,

• Facial nerve injury
vaginal and cervical laceration
• Branchial plexus injury
• Pelvic floor disorders: urinary/anal
• Depressed skull fracture
incontinence, pelvic organ prolapse,
• Corneal abrasion
urinary retention and bladder dysfunction

VACUUM ASSISTED DELIVERY

• Uses vacuum extractor/ventouse to cause gentle suction on fetal scalp that aids in fetal
expulsion
• Theoretical benefits over forceps delivery:
0 simpler requirements for precise positioning of fetal head
0 avoids use of space-occupying blades in the vagina, decrease risk of maternal trauma

I. INSTRUMENT:VACUUMEXTRACTOR
• Contains a cup (metal or plastic), shaft, handle and vacuum generator

KIWI OMNICUP I MITYVAC MYSTIC II

• Contains a handheld vacuum-generating

• Has a soft bell cup attached by a semirigid
pump, which is attached via flexible tubing
shaft to a handheld pump
to a rigid plastic mushroom cup

Shaft

I
Vacuum
Handle generator
I
Vacuum
Handle generator

II. MORBIDITY& COMPLICATIONS

• Avoid using vacuum device to assist delivery <34 weeks AOGdue to possible risk of birth
injuries in preterm infants
• Prior scalp sampling or multiple attempts at fetal scalp electrode placement are relative
contraindications due to possibility of scalp trauma
• Perinatal injuries associated with vacuum extraction compared to forceps delivery:
° Cephalhematoma
Subgaleal hemorrhage
Retinal hemorrhage
Neonatal jaundice secondary to these hemorrhages
Shoulder dystocia
Clavicular fracture
Scalp lacerations

Source:Cunningham
FG,et al. Williams
Obstetrics;2018
148
II. TECHNIQUE(Remember A·B·C·D·E·F·G-H-1-J)
• Adequate pain relief
Anesthesia
• Analgesia is not essential but is recommended, if available
A s· tan e Neonatal support
Au horiz tion • Informed consent
• Bladder should be empty
Bladder
• May do straight catheterization
Cervix • Cervix must be fully dilated, and membranes ruptured

Determine

Equipment
• Position, station and pelvic adequacy
• Think possible shoulder dystocia
• Make certain that the vacuum cup, pump and tubing are
I
'. ·
functioning properly 7 ;
--------1-----------------------------1
posterior fontanelle
• Position the cup over the
• The cup is applied by compressing it in an anteroposterior diameter
Fontanelle and then introducing it into the posterior fourchette while protecting
maternal tissues and making space with the opposite hand
• Sweep finger around cup to clear maternal tissue
• 100 mm Hg initially and between contractions
• Pull with contractions only
• As contraction begins:
Gentle traction 0 Increase pressure to 600 mmHg
0 Prompt the woman for good expulsive effort
0 Traction in axis of birth canal
• No progress with 3 traction-aided contractions
Halt • Vacuum pops off3 times
• No significant progress after 20 minutes of operative vaginal delivery
Incision • Consider episiotomy iflaceration imminent
Jaw • Remove vacuum when fetal jaw is visible, or delivery assured
of Canada;2012-2013
andGynecelogists
Source:ALARM.Societyof Obstetricians

149
 SECTION THREE
BREECH DELIVERY

OVERVIEW OF THE MANAGEMENT OF BREECH PRESENTATION

• Occurs when the breech (fetal buttocks) or lower extremities present into the pelvis
• Types of breech (e.g., frank complete, incomplete) are discussedin previous chapter
• Possible strategies for breech:
Vaginal breech delivery
External cephalic version (ECV) before labor
Planned cesarean birth

I. VAGINAL DELIVERY IN BREECH:

• May be attempted for frank/complete breech presentations
• May be carried out through:
Spontaneous breech delivery
0 Partial breech extraction (PBE)
° Complete breech extraction (CBE)

II. CESAREAN SECTION (CS)

• Planned cesarean delivery for breech:
Lower risk of perinatal morality compared with planned vaginal delivery
0 Lower risk of"serious" neonatal morbidity
0 Not associated with a reduction in the rate of death or developmental delay

Factors Favorina Cesarean Section (CS) of the Breech Fetus

• Lack of operator experience
• Patient preference
• Large fetus >3800-4000 g
• Healthy & viable preterm fetus either with active labor or with indicated delivery
• Severe fetal-growth restriction
• Fetal anomaly incompatible with vaginal delivery
• Prior perinatal death or neonatal birth trauma
• Poor obstetric history (e.g., miscarriages, infertility, etc.)
• Incomplete or footling breech presentation
• Hyperextended head
• Pelvic contraction or unfavorable pelvic shape determined clinically
• Prior CS
Source:Cunningham
FG,et al. WilliamsObstetncs;
2018

III. VERSION
• Fetal presentation is altered by physical manipulation, either by substituting one pole of
a longitudinal presentation for the other, or converting an oblique or transverse lie into a
longitudinal presentation.
• It is simply changing an unfavorable presentation to a favorable one

A. Internal Podalic Version

0 Oblique or cephalic presentation is converted into double footling
0 The only accepted indication is the delivery of the second of twin
0 Membranes preferably still intact, a hand is inserted into the uterine cavity to turn the
fetus manually
0 Seizes one or both feet & draws them through the fully dilated cervix, while the other hand
transabdominally pushing the upper portion of the fetal body in the opposite direction

B. External Cephalic Version (ECV)

° Changing positions from a breech presentation to a cephalic presentation
0 Performed exclusively through the maternal abdominal wall (manipulation through
the anterior abdominal wall only)
0 Performed in a facility with access to stat CS
0 Perform ECVbefore labor and before 36 weeks AOG,but not in very early gestation
150
 • Multiparity • Placental abruption
• Abundant amniotic fluid • Uterine rupture
• Unengaged presenting part • Fetomaternal hemorrhage
• Fetal size 2,500 to 3,000 grams • Alloimmunization
• Posterior placenta • Preterm labor
• Non-obese patient • Fetal compromise or death
• Amniotic fluid embolism
• Non-reassuring fetal heart rate patterns

Procedure

■
Done Before ECV:
• Sonographic examination to check the following:
° Confirm nonvertex presentation
0Amniotic fluid adequacy
0Exclude fetal anomalies
0Placental location
• Fetal heart rate monitor
• Anti-D lg given to Rh-D (-) women
• Administer betamimetics (e.g. terbutaline 250 mcg SC,salbutamol)

• Forward roll of the fetus is attempted first, each hand grasps one fetal pole, and the fetal
buttocks are elevated from the maternal pelvis and displaced laterally
• Buttocks gently guided toward the fund us, while the head is directed toward the pelvis
• Backflip is attempted if forward roll is unsuccessful
• Discontinue when there is excessive discomfort, persistently abnormal fetal heart rate,
or multiple failed attempt

Contraindications to ECV:
ABSOLUTE CONTRAINDICATIONS I RELATIVE CONTRAINDICATIONS

• Placenta previa • Early labor

• Abnormal fetal heart rate pattern • Oligohydramnios
• Compromised fetus • Rupture of membranes
• Active genital herpes simplex virus • Known n uchal cord
• Previous classical uterine incision • Structural uterine abnormalities
• Other uterine surgery that would increase • Fetal-growth restriction
the risk of uterine rupture (e.g. hysterotomy, • Prior abruption or its risk
myomectomy,fullthickness uterine wall incision) • Hyperextension of fetal head
• Antepartum hemorrhage • Morbid maternal obesity
• Multiple gestation (except delivery of
second twin)
Source:CunninghamFG,et al. WilliamsObstetrics;
2018
ALARMCourseManual.TheSocietyof Obstetricians
andGynecologistsof Canada;2012-2013

151
VAGINAL BREECH DELIVERY
• Decision regarding the mode of delivery should depend on the experience of the health
care provider
• Planned vaginal delivery of a term singleton breech fetus may be reasonable under
hospital-specific protocol guidelines

I. CARDINALMOVEMENTSIN BREECH
1 · EN;;s~EE~~NT & I 2. INTERNAL ROTATION I J. LATERAL FLEXION

• 45 degree rotation of hip

• Bitrochanteric diameter in
• Anterior hip toward pubic
oblique diameter • Posterior hip over the
arch
• Anterior hip descends perineum
• Bitrochanteric diameter in
more rapidly
AP diameter of outlet

4. EXTERNAL ROTATION I 5. IN°TERNAL ROTATION I 6. EXPULSION

• Posterior neck under

• Bisacromial diameter in symphysis
• Fetal back turns anteriorly
AP plane • Head born inflexion

152
II. PLANNED VAGINAL BREECH CRITERIA:
Skilled OB,anesthesiologist, and delivery room staff
No contraindication to attempted vaginal birth
Facilities for possible CS available
Patient is informed of risks
EFW: 2500-4000 g
Frank or complete breech
Flexed fetal head
Absence of fetal anomalies (e.g., hydrocephalus)
Continuous fetal heart monitoring
Induction is not recommended
• Oxytocin augmentation if with hypotonic uterine dysfunction
• Passive 2nd stage without active pushing for 90 min allowing breech to descend into pelvis
• Once active pushing commences & delivery not imminent after 60 min, CSis recommended

III. TYPES OF VAGINAL BREECH DELIVERY

TYPES I REMARKS
• Expelled by natural forces of the mother with no assistance, other
I
.

Spontaneous
than support of the baby as it is born
Breech Delivery
• Occurs infrequently and may happen in multi paras
• Delivered by natural forces as far as the umbilicus
• Rest of the body is delivered by the obstetrician
Partial Breech • Delivery ofaftercoming head using (discussed below):
Extraction 0 Mauriceau-Smellie-Veit maneuver
0 Piper Forceps
0 Modified Prague Maneuver

Frank Breech
Extraction

• Delivered by natural forces as far as the hips

• Moderate traction is exerted by a finger in each groin and aided by a
generous episiotomy
• Pinard maneuver for frank breech decomposition: two fingers are
inserted along one extremity to the knee, which is then pushed
away from the midline after spontaneous flexion. Fetal foot may be
grasped and brought down (see illustration)
• Once breech is pulled through the introitus, the steps for partial
breech extraction are applied
• Delivered by extraction (in all steps, we assist the delivery)
• Both feet grasped through the vagina and feet brought through the
Complete Breech
introitus with gentle traction
Extraction
• Once the breech is pulled through the introitus, the steps for partial
breech extraction are then similarly applied and completed
Source:Cunningham
FG,et al. WilliamsObstetrics;
2018

153
IV. BREECHDELIVERYSTEPS
A. General Steps of Breech Delivery
Anesthesia • Request for anesthesia
Episiotomy • Do episiotomy
Spontaneous • Partial breech extraction
delivery • Wait! Don't pull! Hold baby until umbilicus is delivered
Legs • Pinard: lateral rotation of thighs, flex knees
• Delivery when wing of scapula is seen
Arms • Rotate arm to anterior
• Loveset maneuver
Nape • Fetal body rests on arm and apply suprapubic pressure
• Mauriceau-Smellie-Veit maneuver
Aftercoming
• Modified Prague Maneuver
head
• Piper Forceps
Inspect • Check for fetal fractures/injuries or perineal lacerations
Source.ALARM.TheSocietyof 0bstetnc1ansand Gynecologists ofCanada,2012-2013

• Index and middle finger of one hand

are applied over the maxilla, to flex
the head
• Fetal body rests on the palm of the
same hand and forearm
Mauriceau-
• Gentle suprapubic pressure
Smellie-Veit
simultaneously applied by an
maneuver
assistant helps keep the head flexed
• Two fingers of the other hand grasp
the shoulders on both sides of the
neck applying a downward followed
by an upward traction

• Performed when the back of the

fetus fails to rotate to the symphysis
Modified • Two fingers of one hand grasp the
Prague shoulders on both sides of the neck
Maneuver of the back-down fetus from below
while the other hand draws the feet
up and over the maternal abdomen

• Blades of the Piper forceps applied

sequentially on both sides of
the fetal head while an assistant
Piper positions the body with feet pulled
forceps in an upward position
(Laufe- • Piper forceps have a downward
Piper arch in the shank to accommodate
Forceps) the fetal body & lack a pelvic curve
• The head is delivered by pulling the
forceps gently outward and slightly
raising the handle simultaneously

154
C. Maneuvers in the Management of Head Entrapment
MANEUVER I PROCEDURE I FIGURE

• Incision done at the 2, 10 and 6

o'clock position of the cervix
• Avoid cutting at the 3 and 9
Diihrssen
o'clock position to minimize
incisions
injury of the laterally located
cervical branches of the uterine
artery

I
• Under local anesthesia, the
symphyseal cartilage is
Symphysiotomy
divided surgically to widen the
symphysis pubis up to 2.5 cm

Source:Cunningham
FG,et al. WilliamsObstetrics;
2018

15S
 SECTION FOUR
CESAREAN SECTION
CESAREAN SECTION (CS)
• Fetus is delivered through an incision on the anterior uterine wall accessed through
an incision on the maternal abdominal wall
• Causes for 85% of CS: prior CS, dystocia, fetal jeopardy, abnormal fetal presentation

I. DEFINITIONOF TERMS
TERMS I DEFINITION
Laparotomy • Abdominal wall incision to gain access into the intrabdominal cavity
Hysterotomy* • Uterine wall incision to gain access into the intrauterine cavity
Cesarean section • Uterine wall incision specifically done to deliver a fetus of viable AOG
'The termis alsousedto referto a uterineincisionperformed
to delivera nonviable
fetusformaternalindications

II. INDICATIONSFORCS
• Prior cesarean delivery (depending on type, number, and indication)
• Abnormal placentation
• Prior classical hysterotomy
• Unknown uterine scar type
• Uterine incision dehiscence
• Prior full-thickness myomectomy
• Genital tract obstructive mass
• Invasive cervical cancer
• Prior trachelectomy
Maternal
• Permanent cerclage
• Prior pelvic reconstructive surgery
• Pelvic deformity
• HSVor HIVinfection
• Cardiac or pulmonary disease
• Cerebral aneurysm or arteriovenous malformation
• Concurrent pathology requiring intraabdominal surgery
• Perimortem cesarean delivery
• Maternal request*
• Cephalopelvic disproportion
Maternal-Fetal • Failed operative vaginal delivery
• Placenta previa or placental abruption
• Non-reassuring fetal status
• Malpresentation
• Macrosomia
Fetal • Congenital anomaly
• Abnormal umbilical cord Doppler study
• Thrombocytopenia
• Prior neonatal birth trauma
'If a patientrequestsforCesareansectionwithouta clearindication,
reasonforrequestshouldbe examined,
discussed
anddocumented.Thediscussionshouldincludethe overallbenefitsand risksofcesareandeliverycomparedwith
vaginalbirth.
Source:Cunningham
FG,et al.Williams
Obstetrics;
2018
POGS.CPGon Cesareansection.2012

156
III. TECHNICAL ASPECTS OF CS
A. Types of Uterine Cesarean Incisions (Hysterotomy)
0 The type of CS is determined by the incision on the uterus, and not the abdomen
0 May be classified as:
• Lower segment incision (transverse or vertical)
• Classical cesarean incision

CLASSICAL CS ~
• Upper segment is incised
longitudinally from
above the lower segment
upwards to about 10 cm
_____
1--(_m_o_r_e_o_r_I_e_ss_)
• Preferred over classical incision because it has low
tendency to rupture in the next pregnancy (subsequent
VBAC possible)
• Kerr Incision is preferred since there is only moderate
__________
t-_d_i_ss_e_c_ti_o_n_o_f_t_he_b_Ia_d_d_e_r_,..... ~;
I
· ·
;

Advatanges
• Less blood loss
• Any fetus can be
• Placenta is rarely incised
delivered, regardless of
• Fetal head is easier to extract if fetus is in vertex position
orientation in uterus or
• Uterine muscles easier to approximate
gestational age
• Less incidence of uterine rupture
Disadvantages
• Greater blood loss
• Higher risk of post-
operative adhesions • Risk of bladder injury
• Contraindicated to VBAC • Lower uterine segment must be formed
• Increased risk of uterine
rupture

157
 • A straight incision
• Also called the that is 3 cm below
• Also called the median transverse supra pubic the line joining both
infraumbilical longitudinal incision incision or "bikini" anterior superior
• Incision begins 2-3 cm above the incision iliac spines.
superior margin of the symphysis • Preferred for aesthetic • Advantages over
and 12-15 cm in length reasons Pfannenstiel include:
• Quickest to make • Low curvilinear 0Shorter duration of
• Allows faster abdominal entry, incision made at the surgery
causes less bleeding and superficial level of the pubic 0Less blood loss,
nerve injury, and can be easily hairline, 3 cm above fever, and pain
extended cephalad if more space is the superior border of ° Fewer analgesic
required for access symphysis pubis requirements
• 12-15 cm in length 0Shorter
hospitalization

Midline ~~-1---+ Joel-Cohen

vertical ~,......,'--+--+ Pfannestiel

158
VAGINAL BIRTH AFTER CESAREAN (VBAC)
• Describes a vaginal delivery in a woman who has given birth via CS in the past
• May be considered in patients with:
Baby on vertex presentation
,;2 previous low transverse uterine scar (2 previous transverse CS should be offered
and counseled regarding VBAC)
No contraindication to vaginal birth
Operative records which may include opinion of the obstetrician of previous delivery
Source:
AGOG.Practice
BulletinNo.205.2019

If the patient has had one previous CS, would she still be able to deliver vaginally?
• It depends on the type and on the reason why the CSwas done in the first place
• If the CS was a low transverse incision, a VBACmay be considered
• If the reason is a non-permanent indication, a VBACmay be considered (i.e., placenta
previa, non-reassuring fetal status, malpresentation)
• If the reason is a permanent indication, VBACis contraindicated (i.e., contracted pelvis,
pelvic deformity)
I .

I. FACTORSTHAT INFLUENCETRIAL OF LABORIN A WOMANWITH PRIOR CS

• Factors to consider in patient selection for VBAC:
Type of prior uterine incision
lnterdelivery interval (3-fold increase if <18 months interval)
Number of prior CS
Indication of previous CS
A previous vaginal delivery is the most favorable prognostic factor

A. Low versus High Risk

LOW RISK I HIGH RISK*

• Transverse incision • Classical or T incision

• Prior vaginal delivery • Prior rupture
• Appropriate counseling • Patient refusal or inadequate facilities
• Sufficient personnel/equipment • Transfundal surgery
• OB contraindication (e.g., previa)
'Presenceof highriskfeatures:maybe considered
as absolutecontraindications
to VBAC

B F Aff VBACO
INCREASES LIKELIHOOD OF
SUCCESSFULVBAC
I DECREASES LIKELIHOOD OF
SUCCESSFULVBAC

• Previous successful VBAC • Previous CS done for • Estimated birth

• Previous vaginal delivery dystocia weight weight
• Favorable cervix • Need for induction of labor >4,000 g
• Spontaneous labor requiring cervical ripening • Maternal BM! >30
• Non-recurrent indication for • Need for augmentation of • Hypertension
previous CS labor
• Maternal age <40 years • Gestational age >40 weeks
Source:AGOGCommittee
OpinionNo.761.2019
II. PREREQUISITESOF VBAC
Informed consent of the patient
Previous low transverse cesarean section (LTCS)(KERR Incision)
Nonrepetitive indication for CS
No pelvic contracture
Continuous electronic fetal monitoring
Availability to perform an emergency repeat CS within 30 minutes of decision to operate
Access to blood products

III. CONTRAINDICATIONSTO VBAC

• Previous classical or "T" incision
• Prior uterine rupture
• Contraindication for vaginal delivery (e.g., placenta previa)
159
 SECTION FIVE
OBSiTETRIC ANALGESIA AND ANESTHESIA

REGIONAL ANESTHESIA
• Most commonly used technique in obstetric procedures
• Includes subarachnoid block, epidural block, peripheral nerve block

I. TYPES OF REGIONAL ANESTHESIA

TYPE I REMARKS I USES
• Mainlyin the second stage of labor
• Delivered near the ischial
• Episiotomy and episiorrhaphy
tuberosity
Pudenda! Block • Vulvar excision procedures
• A spinal needle or a trumpet
(e.g., Bartholin cyst excision,
is used
marsupialization, etc.)
• Cesarean section
• Exploratory laparotomies
• Used for laparotomies
• Total abdominal hysterectomy
• Can achieve both sensory and
Subarachnoid with bilateral salpingo-
motor block
Block or Spinal oophorectomy (THBSO)
Anesthesia • Saddle block: form of spinal
• Uncomplicated ectopic pregnancy
anesthesia confined to the
• Vulvar excision procedures
sacral nerve roots
(e.g., Bartholin cyst excision,
marsupialization, etc.)
• Labor analgesia for vaginal
• Segmental blockade
deliveries
• Involves placing a catheter in
• Anticipated long or extended
the epidural space, close to
surgeries (e.g., complicated
the nerve roots
ectopic pregnancies, etc.)
• Doses can be given gradually
Epidural • Can be used when a planned
or in increments (unlike that
vaginal delivery is converted to
of spinal)
cesarean section
• Sensory and/or motor block
• High risk pregnancies (patients
can be achieved in a dose
with heart failure, congenital
dependent manner
heart diseases)
• Paravertebral
• Paracervical block
Others
• Combined spinal-epidural: takes the advantages of both spinal and
epidural anesthesia

II. SPINAL VERSUS EPIDURAL BLOCKS

PARAMETERS
I SPINAL
I EPIDURAL
• Anesthetics are given in the • Anesthetics are given in the
Technique
subarachnoid space epidural space, above the dura
• Rapid onset of action (less than
Onset of action • Slower onset of action
5 minutes)
• May give intermittent and
Dosing • Single-dose anesthetic
repeated doses
• May extend the duration of
Duration • Shorter anesthetic duration block by giving additional doses
through the epidural catheter

160
III. LANDMARKS
A. Iliac Crest
0 Transverse line connecting highest points of iliac crest (Tuffier line)
0 At L4-LS intervertebral space where lumbar puncture is usually done, and spinal
anesthesia is introduced
• Saddle and epidural block can also be given in this area

B. Lumbar Puncture
° Common vertebral level: L4-LS interspace
0 Avoids injury to the spinal cord

IV. CONTRAINDICATIONS TO REGIONAL ANESTHESIA

• No consent*

I
• Skin infections at puncture site*
• Clotting defect
• Hypovolemia / dehydration / shock
• Sepsis
• Increased intracranial pressure (risk of herniation)
• Neurologic diseases (including psychiatric diseases)
• Deformities of spine or vertebral column
• Prolapsed vertebral disk
•Absolutecontraindications
to regionalanesthesia

V. APPLICATIONS OF REGIONAL ANESTHESIA

A. Vaginal Delivery
APPLICATION I REMARKS
I OPTIONS
• Pain is due to uterine
contraction & cervical dilatation
1st stage of • Intravenous sedation
which is innervated by the
labor • Epidural block
sympathetic thoraco-lumbar
spinal nerves (TlO-Ll)
• Intravenous sedation
• Pain is due to distention of
2nd stage of • Epidural block
pelvic structures and perineum
labor • Pudenda! block
• Sacral nerves S2-S4 are involved
• Saddle block

B. Cesarean Section (CS)

OPTIONS
I REMARKS
Spinal • Block height should at least be at T6 level
anesthesia • Usual choice of anesthesia for short uncomplicated surgeries
• Block height should at least be at T6 level
• Both sensory & motor block can be achieved in a dose dependent manner
Epidural
• Ideal for post-operative pain control
anesthesia
• Additional doses of anesthetics can be added if surgery is longer than
expected
• Used in cases when CS has to be performed urgently or if there is not
General enough time to administer regional anesthesia
inhalational • Patient is rendered unconscious throughout the surgery
anesthesia • Patient is intubated and respiration is controlled
• Baby has to be delivered at the soonest to avoid neonatal depression
• Given in conjunction with either regional or general anesthesia
• Used to minimize adverse side effects of individual anesthetics like
Adjunct drugs
vomiting, salivation, hypotension and bradycardia while affording
longer pain control

161
VI. FREQUENTLYUSED DRUGS IN REGIONALANESTHESIA:
DRUGS
I ONSET I DURATION
I CLINICAL USE
• Epidural for cesarean & labor
• 3 hours
• 4-10 analgesia
Bupivacaine • Extended to 4 hours if
minutes • Spinal for CS
with epinephrine wash
• Saddle block for vaginal delivery
• 2-2.5 hours
• 2-10 • Low spinal block
Tetracaine • Extended to 3 hours if
minutes • Spinal for CS
with epinephrine wash
• Limited to 1.5 hours
• 1-3 • Pudenda! block
Lidocaine • Extended to 2.5 hours if
minutes • Epidural for CS
with epinephrine wash

VII. COMPLICATIONSOF REGIONALANALGESIA

• Hypotension
• Nausea and vomiting
• Post dural puncture headache
• High spinal anesthesia
• Inadvertent intrathecal, subdural or intravascular injection of local anesthetic drugs
• Epidural hematoma
• Epidural abscess
• Infection from puncture site
• Spinal nerve injury
• Local Anesthetic Systemic Toxicity (LAST)
ANESTHETIC
AGENT
ICENTRAL NERVOUS SYSTEM
TOXICITY*
I CARDIOVASCULAR
TOXICITY*
• Lightheadedness Initial (stimulation):
Aminoesters
• 2-Chloroprocaine • Dizziness • Hypertension
• Tinnitus • Tachycardia
• Metallic taste
• Numbness of tongue & mouth Late (depression):
Aminoamides • Slurred speech • Hypotension
• Bupivacaine • Muscle excitation & • Arrhythmia
• Lidocaine fasciculation • Impaired uteroplacental
• Ropivacaine • Generalized convulsions perfusion develops only at
• Loss of consciousness higher serum levels
'Centralnervoussystemsymptomsusuallymanifestsbeforecardiovascular
symptoms

162
GENERAL ANESTHESIA
• Includes inhalation and intravenous types
• Usually avoided because of greater risk for mother and baby during procedure
• Complications
• Mendelson syndrome (aspiration pneumonitis): a complication from vomiting and
aspiration of gastric contents
• Possibility of anesthetics crossing the placental barrie1; thereby causing
fetal depression

I. TYPES OF GENERALANESTHETICS
ANESTHETIC I REMARKS
Inhalational Anesthetics
Enflurane

Halothane
• Can be used for labor analgesia during vaginal delivery
• No adequate studies in pregnant women
• High risk for uterine atony
I
. '

lsoflurane • Inadequate data for use in obstetrical anesthesia

Nitrous Oxide
• Can be used for labor analgesia
(N2O)
Methoxyflurane • Not used due to nephrotoxicity
• Newer volatile anesthetic (safer)
Sevoflurane • Has a shorter induction and recovery time
• Can also cause uterine atony
Intravenous Anesthetics
• Benzodiazepine
• Used for sedation and anxiolysis
Midazolam
• May cause anterograde amnesia, and respiratory depression at
higher doses
• Short acting opioid
• Rapid onset analgesic
Fentanyl
• Used for balanced anesthesia
• Can cause respiratory depression in higher doses
• Dissociative type anesthetic/ analgesic
Ketamine • Causes increase in blood pressure, increased salivation, and
hallucinations
• Used in short procedures because of its short duration
(about 15 minutes)
Propofol
• Most commonly used intravenous agent for induction of general
anesthesia
• Barbiturate
Thiopental Na•
• Used for induction of general anesthesia
• Used to facilitate vocal cord and muscular paralysis to aid in
Neuromuscular intubation
blocking agents • Do not cross the placenta
• Examples include succinylcholine, rocuronium

163
REFERENCES
l.ACOG Practice Bulletin No. 205: Vaginal birth after cesarean delivery. (2019). Obstetrics & Gynecology, 133(2), el 10-e127.
https://doi.org/10.1097 / AOG.0000000000003078
2.ACOG
CommitteeOpinionNumber761. Cesareandeliveryon maternalrequest.January2019
3.Advancesin Labour and Risk Management (ALARM) Course Manual, 19th Edition, The Society of Obstetriciansand
Gynecologists of Canada. 2012-2013
4.Barash, P.G. (2017). Clinical Anesthesia 8th edition. Philadelphia: Wolters Kluwer.
S.Chestnut,D.H. (2014). Chestnut'sObstetricAnesthesia:Principlesand Practice5th edition.Philadelphia:ElsevierSaunders.
6.Cunningham, E G., Levene, K J.. Bloom, S. L.. Spong. C. Y.,Dashe, J.S., Hoffman, B. L.,Sheffield,). S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
7.Handa,Victoria L; Van Le, Linda (2019) Te LindesOperativeGynecology12th edition Lippincott Williams & Wilkins
8.Hofmeyr GJ,Shweni PM: Symphysiotomyfor feta-pelvicdisproportion.CochraneDatabaseSystRev 10:CD005299, 2012
9.Hulka,). Glob. libr. women's med.,(ISSN: 1756-2228) 2008; DOI 10.3843/GLOWM.10037
10. LandonMB, HauthJC,LeveneKJ,SpongCY,LeindeckerS,Varner MW, et al. Maternal and perinataloutcomesassociatedwith
a trial oflabor after prior cesarean delivery. N Engl J Med 2004;351(25):2581-9.
11. LandonMB, SpongCY,Thom E, et al: Riskof uterine rupture with a trial of labor in women with multiple and singleprior
cesareandelivery.ObstetGynecol108:12, 2006
12. National Institutes of Health ConsensusDevelopment Conference Panel: National Institutes of Health Consensus
Development conference statement: Vaginal birth after cesarean: new insights. March 8-10, 2010. Obstet Gynecol
115:1279, 2010
13. Operative Vaginal Birth: ACOGPractice Bulletin, Number 219. Obstet Gynecol 2020; 135:el49.
14. Postgraduate Manual of Obstetrics & Gynecology for Practical Examination by By Neerja Goel, Shalini Rajaram, Sandhya
Jain,SumitaMehta
15. Sandberg EC: Shoulder dystocia: associatedwith versus caused by the Zavanelli maneuver. Am J Obstet Gynecol
197(1):115, 2007
16. SOGC.(2010) Advances in Labour and Risk Management Textbook (ALARM)Course Syllabus. Operative Vaginal Delivery.
SOGC.Ottawa, Ontario
17. SOGC.(2010} Advances in Labour and Risk Management Textbook (ALARM) Course Syllabus. Vaginal Breech Delivery.
SOGC.Ottawa, Ontario
18. The Societyof Obstetriciansand Gynaecologists of Canada.Advancesin Labourand RiskManagement.19th Edition.2012-
2013
19. Yeomans ER. Hoffman BL, Gilstrap LC, Cunningham FG. Cunningham and Gilstrap's Operative Obstetrics (3rd Ed).
McGraw-Hill Education. 2017

164
PUERPERIUM
AND
POSTPARTUM
COMPLICATIONS
 SECTION ONE
THE PUERPERIUM
THE PUERPERIUM (POSTPARTUM PERIOD)
• From Latin "puer" (child)+ "parus" (bringing forth)
• The time after delivery when maternal physiologic changes related to pregnancy return
to the non-pregnant state usually by 6 weeks post-delivery
• Begins as soon as placenta is expelled and lasts for ~6 weeks when uterus regresses to
almost the non-pregnant size

MATERNAL CHANGES DURING THE PUERPERIUM

• By 6 weeks after delivery, most of the changes of pregnancy and labor have resolved and
the body has returned to its non pregnant state
• Involution: process whereby the reproductive organs return to their nonpregnant state

Summary of Anatomic Changes during Puerperium

DIVISION
I BIRTH CANAL
I CERVIX
I UTERUS
I
PLACENTAL
SITE
I
• Becomes firm &
• Soft and relaxed retracted with
• Contracts
immediately alternate hardening
rapidly
after birth & softening
• Vagina is • Raised surface
Immediate • Begins to • Fundus lies
greatly • Measures~ 7.5
(within 24 contract slowly just below the
distended with cm (palm-size)
hours) • Cervical as umbilicus
smooth walls • Consists of
(dilated at 10 • Lower segment
thrombosed
cm) closes becomes thin, and
vessels
gradually collapsed
• Weighs ~1000 g
• Fundus descends
halfway between
• Remains • Decreases in
symphysis pubis
edematous and size: ~3-4 cm
and umbilicus
thin for several by the end of
• Within 2-3 days,
days the 2nd week
• Thickening of the decidua
• Possible to • Initially
Early vaginal mucosa differentiates into
introduce 2 consists of
(up to 7 with return two layers:
fingers into thrombosed
days) of ovarian • Superficial layer
cervical os vessels,
function is sloughed in
for first 4-6 ultimately
the lochia
postpartum days undergoes
• Basal layer is the
(i.e., admits 2 organization
11 source of new
fingers)
endometrium
• Weighs ~500 g
• Vaginal rugae • Complete
• Returns to its
reappear at involution
normal state • Remains
3rd week • Lower segment
at 4 weeks elevated
• lnvolutes over reverts back to
postpartum • Decreases in
Remote 4-8 weeks normal shape &
• External os does size: ~1.5 cm
(up to 6 • Regains tone, size of the isthmus
not completely • Complete
weeks) but never to the • Endometrium at
resume its extrusion of
virginal state the placental site is
pregravid placental site
• Proliferation restored
appearance
of the vaginal • Weighs ~SOg
epithelium
Source:Cunningham
FG,et al. WilliamsObstetrics
25thEdition;2018

167
I. BIRTH CANAL:VAGINA& VAGINALOUTLET
• Early in puerperium, the vagina & its outlet form a spacious, smooth-walled passage that
gradually diminishes in size but rarely return to nulliparous dimensions
• By the 4-6th week postpartum, vaginal epithelium begins to proliferate, coincidental with
resumed ovarian estrogen production
• Lacerations or stretching of the perineum during delivery may result in relaxation of the
vaginal outlet

II. CERVIX
• External os is usually lacerated laterally
• By the end of 1st week:
° Cervical opening narrows, the cervix thickens, and endocervical canal reforms
0External os remains wider and bilateral depressions at the site of lacerations become
permanent (changes characteristic ofa parous cervix)
• Cervical epithelium undergoes considerable remodeling

III. UTERUS
A. Uterine Involution

Delivery day
2 days postpartum
4 days postpartum
6 days postpartum
8 days postpartum

• After placental expulsion, fund us of the contracted uterus lies slightly below umbilicus
• Fundus descends about 1-2 cm every 24 hours
• By 6th postpartum day, fund us is located halfway between symphysis pubis & umbilicus
• It takes up to 8 weeks for the uterine cavity to regress to its nonpregnant state.

B. Lochia
Vaginal discharge from sloughed off decidual tissue which consists of erythrocytes,
0

shredded decidua, epithelial cells, and bacteria

Lochia can persist for up to 4 to 8 weeks after delivery
0

TYPE I DESCRIPTION
• Blood from first few days after delivery
Lochia rubra
• Flow in amounts like a heavy menstrual period
(red)
• Persistence ofred lochia means subinvolution
• From 4 to 12 days (~2 weeks postpartum)
Lochia serosa • Color becomes paler
• Flow is light to moderate in amount
• At about 10th day to 3 weeks postpartum
Lochia alba
• Because of admixture of leukocytes & reduced fluid content, it
(pale white)
assumes a white or yellowish-white color

168
C. Clinical Correlations
I
CORRELATION REMARKS I MANAGEMENT
• Secondary to uterine involution
• Similar to but milder than labor
contractions
• More pronounced as parity increases
and worsens when the infant suckles
0 Primipara: uterus tends to remain
Afterpains tonically contracted after delivery • Analgesics as needed
0 Multi para: contracts vigorously at
intervals similar to (but milder) the
pain of labor contractions
• Occur during the first 2-3 days of
puerperium (intensity decreases after
1st postpartum day)

■
• Arrest or retardation of involution • Methylergonovine (if not
• Suspected when there is prolongation contraindicated)
of lochial discharge and irregular or • Prostaglandin-E analogue
excessive uterine bleeding (e.g., Carboprost,
Subinvolution • Uterus is larger & softer than would be Misoprostol*)
expected • Antibiotics if due to
• Retention of placental fragments, metritis
anemia, and pelvic infection may also • Hematinics if with
cause subinvolution anemia
• Oxytocin
• Methylergonovine (if not
contraindicated)
• Prostaglandin-E analogue
(e.g., Carboprost,
• Bleeding 24 hours to 12 weeks after
Misoprostol*): if
delivery
sonography reveals an
Secondary • Usually due to abnormal involution of
empty cavity
Postpartum the placental site
• Gentle suction curettage if
Hemorrhage • Occasionally due to retention of a
with large clots in cavity
placental fragment or a uterine artery
• Antibiotics for infection
pseudoaneurysm
• Curettage not routinely
performed (it may
worsen bleeding)
• Hematinics if with
anemia
• Misoprostol
is notFDAapprovedforuse in the localsetting

169
IV.LACTATION
• In breastfeeding mothers, lactation is the most dominant physiologic event of the puerperium
• After delivery, estrogen and prolactin levels decrease - however with suckling, amount of
prolactin produced by the pituitary is elevated (let-down reflex)
• Colostrum ( deep lemon-colored liquid) is secreted by the breasts and can be expressed
from the nipple by the second postpartum day and may persists for 5 days to 2 weeks
• Gradual conversion of "transitional milk" to mature milk may take place in 4-6 weeks

I LACTATING
(BREASTFEEDING) MOTHERS*
I NON-LACTATING MOTHERS

• Estrogen and progesterone levels decrease markedly after expulsion of the

Placental
placenta
hormones
• Estrogen in nonlactating women begin to increase by 2 weeks after birth

• By 3 months postpartum, prolactin

levels approaches the non- • Declines, reaching the prepregnant
Prolactin
pregnant state with slight increase range by 2nd to 3rd week postpartum
during suckling
• Varies (may take as long as 6-12 • 70% of non-lactating mothers resume
Menstruation ..
months postpartum) menses by 12 weeks postpartum
• Usually occurs 6 months • May occur as early as 6 weeks
Ovulation••
postpartum postpartum
• Lactatingmother:defined as a motherwho feeds at least 6 episodes of suckling/daytotaling>80 mins in 24 hours
"In breastfeedingmothers,contraceptiveprotectionis about 98% up to 6 months postpartum(i.e., lactation
amenorrhea method or LAM).However,ovulationmay precede the firstmenstrualperiodso it is possible for patient
to become pregnant before she menstruates
Source: Lobo,et al. ComprehensiveGynecology.7th ed; 2017
Stern JM, et al. ClinEndocrinol(Oxf);1986
TysonJE, et al. AmJ Obstet Gynecol;1972

VI. OTHER CHANGES

• Varying degrees of submucosal hemorrhage and edema are seen
• Bladder has an increased capacity and a relative insensitivity to intravesical
Urinary tract pressure
• Dilated ureters and renal pelvis return to their pre-pregnancy state 2-8
weeks postpartum

• Abdominal wall remains soft and flaccid (recovery is aided by exercise)

Peritoneum
• Striae gravidarum (stretch marks): reddish streaks found in the skin over the
&abdominal
abdomen, breasts and thighs
wall
• Diastasis recti: marked separation of rectus muscle when it remains atonic
• Marked leukocytosis & thrombocytosis during and after labor
• WBC count sometimes reaches 30,000/uL due to granulocytosis
Hematologic • Relative lymphopenia and absolute eosinopenia
changes • Hemoglobin and hematocrit fluctuate moderately (if it decreases
significantly, a considerable amount of blood has been lost]
• One week after delivery, blood volume may return to prepregnant levels
- • Cardiac output and heart rate remain elevated for 24-48 hours postpartum
and declines to nonpregnant values by 10 days.
Fluids and
• Systemic vascular resistance steadily increase > 2 days postpartum
hemodynamics
• Postpartum diuresis occurs between 2nd and 5th days
• Blood volume returns to normal levels by 1st or 2nd week after birth

• Upon delivery: ~5.4 kg is lost

Weight loss • Two weeks postpartum: 4 kg is lost
• Two weeks to 6 months: 2.5 kg is lost
Source: CunninghamFG, et al. WilliamsObstetrics25th Edition;2018

170
POSTPARTUM CARE
I. HOSPITALCARE(FACILITY-BASED)
ASPECT I REMARKS
• BP and pulse every 15 minutes for the first 2 hours after delivery
• Temperature every 4 hours for the first 8 hours after delivery
• Amount of vaginal bleeding
• Uterus is closely monitored at least 1 hour after delivery
Monitoring
° Fund us palpated to ensure that it is well contracted
0 If there is relaxation, it should be massaged through abdomen until it is
contracted
• Take note if regional anesthesia or general anesthesia was used
• Should be done as soon as possible
0 Vaginal delivery: ambulate within 12 to 24 hours
° Cesarean delivery: ambulate after 24 hours

■
Early • _Advantages of early ambulation:
ambulation ° Fewer bladder complications
0 Less frequent constipation
0 Reduced puerperal venous thrombosis
0 Reduced pulmonary embolism
• Cleanse vulva from anterior to posterior, toward the anus
• Ice bag applied to the perineum may reduce edema & discomfort from a
laceration or episiotomy
• Local anesthetic spray may also provide periodic relief; analgesics if needed
Perinea[ • Severe perinea!, vaginal, or rectal pain always warrants careful inspection
care and palpation, and may indicate:
0 Hematoma (if within 24 hours postpartum)
0 Infection after 3rd or 4th day
• Episiotomy incision normally is firmly healed and nearly asymptomatic by
the 3rd week
• If abdomen is unusually flabby or pendulous, an ordinary girdle is often
Abdominal s.atisfactory
wall • Exercise to restore abdominal wall tone may be started any time after
relaxation vaginal delivery and as soon as abdominal soreness diminishes after
cesarean delivery
• Uncomplicated vaginal delivery: may be given food after 2 hours with no
dietary restrictions
Nutrition
• Increased caloric and protein requirements because of lactation.
• Continue iron supplementation for at least 3 months after delivery
Bladder
• Urinary retention & bladder overdistention: common in early puerperium
function
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018

II. HOMECARE
• May resume after 2 weeks based on desire and comfort
Coitus
• Hypoestrogenic state may cause dryness, requiring vaginal lubricants
Common • Fatigue, breast problems, anemia, backache, hemorrhoids, headache,
morbidity "blues", constipation, suture breakdown, and vaginal discharge
• Uncomplicated vaginal delivery: can resume most activities like bathing,
Follow-up driving, household chores
care • Postpartum visit: maybe done 1 week after to identify early problems,
then 4-6 weeks after to initiate contraceptive practices
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018
171
POSTPARTUM HEMORRHAGE
Discussed in detail in Chapter 7

I. DEFINITIONS
Postpartum • ;,1000 mL blood loss after completion of the third stage of labor with
Hemorrhage signs and symptoms of hypovolemia
• Bleeding after 24 hours to 12 weeks after delivery
• May be due to abnormal involution of placental site or retention of
Late placental tissue (e.g., placental polyp)
postpartum • Initial treatment: medical control of bleeding (e.g., oxytocin, ergonovine,
hemorrhage prostaglandins)
• Curettage is carried out only if appreciable bleeding persists or recurs
after medical management

II. OVERVIEWOF THE COMMONCAUSESOF POSTPARTUMHEMORRHAGE

I DESCRIPTION
I MANAGEMENT
• Uterotonic agents
• Bimanual uterine compression
• Most frequent cause of • Tamponade (e.g.. Bakri balloon)
obstetrical hemorrhage • Surgical procedures
Uterine atony • Inability of the uterus to 0 Uterine compression sutures (e.g.,
contract sufficiently after 8-Lynch sutures)
delivery 0 Pelvic vessel ligation (internal iliac)
0 Angiographic embolization
0 Total or subtotal hysterectomy
• May be cause by • Gentle suction cur!;!ttage (if with
Placental site retention of a placental sonographic evidence retained
subinvolution fragment or uterine artery placental fragments/blood clots)
pseudoaneurysm • Uterotonic agents
• Primary: rupture of a
previously unscarred uterus
Uterine • Uterine repair
• Secondary: rupture due to a
rupture • Total or subtotal hysterectomy
preexisting incision, injury
or myometrial abnormalities
Uterine • Uterine fundus turns partially • Manual repositioning of uterine fund us
inversion or completely inside out • Surgery
• Suturing of lacerations
• Includes vulvovaginal and
Genital tract • Large, expanding hematomas
lacerations & puerperal
trauma repaired surgically by evacuating
hematomas
clots and ligating bleeding vessels
• Intravascular activation of
Consumptive
clotting • Prompt identification and removal of
Coagulopathy
• Most common cause: the cause of the coagulopathy
or DIC
placental abruption
Source:Cunningham
FG,et al.WilliamsObstetrics
25thEdition;2018

172
III. UTEROTONIC
AGENTS
• Uterotonics are pharmacologic agents that induces uterine contractions are given for the
prevention and treatment of postpartum hemorrhage

MECHANISM OF
AGENT
I ACTION
I DOSE
I REMARKS
.,
First Line
• Binds to oxytocin
• Prevention: 10 lU IM • Overdose or
receptors in the
or 5-10 !U IV bolus prolonged use
myometrium
• Treatment: 20-40 lU can cause water
stimulating
Oxytocin + lL normal saline: intoxication
contractions
infuse 500 mL over • Possible hypotension
by increasing
10 mins, then infuse with IV use following
permeability of
at 250 mL/hr cesarean delivery
uterine myofibrils

■
I>
Second{.ine r:I .~ .,.,
Methyl- • Ergot alkaloids • Used as second line to
• Treatment: 0.2
ergonovine & increase uterine treat uterine atony
mg IM, every 2
Ergonovine muscular tone by • Do not give IV since it
to 4 hours if with
(Ergot causing sustained may cause dangerous
Alkaloids) bleeding
uterine contractions hypertension
• Maybe given during
• Prevention: delivery of the
125 ug IM anterior shoulder
• Treatment: • Should not be used
• Prostaglandin F2 250 ug IM & may for women with
Carboprost
alpha analogues be repeated at asthma, preeclampsia
15-90-minute or those suspected
intervals up to a for amniotic fluid
maximum of8 doses embolism.
• May cause diarrhea
• Prevention: 600mcg
orally • Caution in those with
• Prostagladin El • Treatment: 800 to cardiovascular disease
Misoprostol*
analogue 1000 mcg rectally • Side effects include
or 600 to 800 mcg shivering and fever
sublingually
• Long acting
analogue of oxytocin
with agonist
properties
• Binds to oxytocin
receptors in uterine • Can cause
smooth muscle hypotension and
• 100 mcg IV over 1
Carbetocin resulting in: tachycardia
minute
0 Rhythmic • Can cause water
contractions retention
0 Increased

frequency of
contractions
0 Increased uterine
tone
• Misoprostolis not FDAapprovedforuse in the localsetting
Source:CunninghamFG,et al. WilliamsObstetrics25th Edition:2018;EvensenA, et al. AmFam Physician;2017
WHO;2018
173
PUERPERAL INFECTIONS
• General term used to describe any bacterial infection of the genital tract after delivery
• Part of the lethal triad of maternal death (puerperal infections, preeclampsia, and
obstetrical hemorrhage)

I. PUERPERAL FEVER
• Oral temperature ;c38°C on any 2 of the first 10 days postpartum, exclusive of the first 24
hours, taken at least four times daily
• Most persistent fever after childbirth are caused by genital tract infection
DIFFERENTIALS
I REMARKS

Genital tract infection • Infections involving the perineum, vagina, cervix, and uterus

• Upper urinary tract infection

Pyelonephritis
• Presents as fever, bacteriuria, pyuria & costovertebral angle tenderness
• "Breast or milk fever": temperature does not exceed 39°C and lasts
<24 hours
Breast engorgement
• May give analgesics or antipyretics
• This should be differentiated from infectious mastitis and breast abscess
• Pelvic infection leads to infection of the vein wall and intimal damage
Thrombophlebitis
• Affects both superficial and deep veins
(Rare)
• There is pain or edema on the affected leg or inguinal area
Respiratory • Usually secondary to atelectasis
complications • Occur within first 24 hours following delivery due to hypoventilation

II. PUERPERAL UTERINE INFECTIONS

• Has been called endometritis, metritis, endomyometritis, endoparametritis
• Infection involves not only the decidua, but also the myometrium & parametrial tissues;
therefore, the preferred term is metritis with pelvic cellulitis
A. Etiopathogenesis
1. Risk Factors for Puerperal Uterine Infections
• Route of delivery (most significant factor): greater risk with CS
• Longer duration of labor (especially if there is PROM)
• Premature/prolonged rupture of membranes
• Frequent vaginal examinations during labor and use of internal fetal monitor
• Cervical/vaginal lacerations
• Manual removal of placenta and retained placental fragments or fetal membranes
• Others: anemia, poor nutrition, young maternal age, multiparity, socioeconomic status
2. Pathogenesis
• During labor and delivery, the endogenous cervicovaginal nora migrate into
Vaginal the uterine cavity
delivery • Placental site is composed of necrotic material which provides an excellent
culture media for bacteria.

• The basalis layer of the uterus is iatrogenically disrupted where infection can
Cesarean traverse the layers of the uterus
section • Presence of foreign body (e.g., sutures), myometrial injury, hematomas and
necrosis at the suture line further enhance the potential for infection

3. Microbiology
• Most pelvic infections are caused by bacteria indigenous to the female genital tract
• Bacteria commonly responsible:
• Streptococci,Enterococcus,Gram(-) Bacteria(£ coli,Klebsiella,Proteus),
Aerobes
Staphylococcusaureus,Staphylococcusepidermidis, Gardnerellavaginalis
• Bacteroidesfragilis,Peptococcusspp, Peptostreptococcusspp, Prevotellaspp,
Anaerobes
Clostridiumspp, Fusobacteriumspp, Mobiluncusspp
Others • Mycoplasmaspp, Chalmyd.iatrachomatis.Neisseriagonorrhea
174
 B. Manifestations
° Fever: most important criterion for the diagnosis of postpartum metritis (temperature
commonly exceeds 38°C)
0Abdominal pain, bothersome afterpains, malaise
0Parametrial tenderness
° Foul smelling discharge or lochia
0Uterine or parametrial tenderness on bimanual exam

C. Management
SEVERITY
I MANAGEMENT*
• Oral or intramuscular antimicrobials:
Non-severe
, Ampicillin + Gentamicin, OR
metritis 0 Amoxicillin-clavulanicacid orally q12 x 7 days
Moderate to severe • IV broad-spectrum antibiotics:
metritis (including ° Clindamycin+ Gentamicin (gold standard), PLUS

■
those following CS) 0 Ampicillin(if with sepsis syndrome or suspected enterococcalinfection)
'Improvement
followsin48-72hrs (persistenceof fevermandatessearchforcauses of refractorypelvicinfection)

D. Prevention of Infection
Perioperative antimicrobial
prophylaxis
Operative technique
• Single-dose Ampicillin 2g or first-generation cephalosporin
(e.g.,cefazolin 2 g IVANST)
• Allow placenta to separate spontaneously
• Avoidexteriorizing the uterus to close the hysterotomy
Source:Cunningham
FG,et al. Williams
Obstetrics25thEdition;2018

III. INFECTIONSOF PERINEUM,VAGINA,CERVIX

A. Etiopathogenesis
0 With infection, dehiscence is a concern
0 Vaginal lacerations may become infected directly or by extension from the perineum
° Cervical lacerations are common but seldom are noticeably infected, which may
manifest as metritis
PERINEAL
INFECTION
I DESCRIPTION
I MANAGEMENT

• Infection of episiotomy site • Remove sutures and drainage

• Fourth-degree lacerations is associated • Check for retained foreign bodies
Episiotomy
with infection and dehiscence • If with cellulitis but no purulent
infections
• lntrapartum antimicrobials were discharge:closeobservationand broad
protective spectrum antimicrobial therapy
• Localwound care and intravenous
• Breakdown of previouslyrepaired
antimicrobials
lacerations or episiotomies
• May do early repair of episiotomy
Episiotomy • Most commonly associated with
dehiscence*
dehiscence episiotomy infection
• Localwound care, stool softeners
• Other risk factors: coagulation
and no sexual contact until vagina
disorders, smoking, HPV
and rectum are healed
"Earlyrepairof episiotomy
dehiscenceprotocol:openwound,removesuture,beginintravenousantimicrobials,
woundcare (sitzbath,adequateanalgesiafordebridement,scrubwounddailywithPovidoneiodinesolution),
closurewhenafebrileand the tissueis pinkwithhealthygranulation
tissue,bowelprepforfourthdegreerepair
Source:Cunningham
FG,et al. W1ll1ams
Obstetrics25thEd1t1on;
2018

B. Manifestations
, Local pain and dysuria, with or without urinary retention
Most common findings: pain, purulent discharge, fever
0

Vaginal lacerations may become infected directly or by extension from the perineum
0

° Cervical lacerations are common, and the cervix normally harbors potentially
pathogenic organisms

17S
IV.UTERINE& PELVICINFECTIONS
ETIOPATHOGENESIS
I MANIFESTATIONS
I MANAGEMENT

Abd omma II nc,s,onH_ n ect,ons ..

• Most cornmon cause of persistent • Wound (disruption] dehiscence: • Antimicrobials

fever in women treated for metritis most manifest on the 5th post- • Surgical drainage
• Abscess on the incision site following operative day accompanied by • Debridement of
Cesarean delivery usually cause serosanguinous discharge devitalized tissues
persistent fever or fever beginning • Necrotizing fasciitis: severe
about the fourth day wound infection which
• Risk factors include obesity, diabetes, may involve skin, superficial
immunosuppression, anemia, and deep subcutaneous
and inadequate hemostasis with tissues, and any of the
hematoma formation abdominopelvic fascia! layers
Adnexal (Ovarian) Abscess
• Rarely develops in puerperium • Unilateral • Antimicrobial
• Caused by bacterial invasion through • Usually presents 1-2 weeks therapy
a rent in the ovarian capsule after delivery
• Rupture is common

Peritonitis
,, • Peritonitis may be severe

• Most often caused by uterine • Adynamic ileus may be the • Antibiotics with or
incisional necrosis and dehiscence; first symptom without surgical
others: ruptured adnexal abscess or • Severe pain intervention
inadvertent bowel injury at CS • Abdominal tenderness
Parametrial Phlegmon
• Parametrial cellulitis that forms an • Fever persists > 72 hours • Antibiotics
area of induration (phlegmon) within despite IV antibiotics • Surgery
the leaves of the broad ligament, • CTscan (hysterectomy &
seen in those who develop metritis debridement) for
following Cesarean delivery uterine incisional
• Most common form of extension is necrosis because of
laterally along the broad ligament. ileus & peritonitis
with a tendency to extend to the • CT-directed needle
pelvic sidewall aspiration
Septic Pelvic Thrombophlebitis
• Arises as an extension along venous • Presence of metritis with • Antibiotics
routes and may cause thrombosis. fever despite ;eS days of
• Puerperal septic thrombophlebitis is appropriate antibiotics
likely to involve one or both ovarian • Abdominal pain & chills
venous plexuses because they drain • Diagnosis confirmed by
the upper uterus and therefore the either pelvic CT or MRI
placental implantation site
Toxic.ShockSyndrdlne .

• Acute febrile illness with severe • Fever. headache, confusion, • Supportive (principal
multisystem derangement diffuse macular erythematous therapy]
• Most common etiologic agent: rash, subcutaneous edema, • Antibiotics
Staphylococcus aureus, exotoxin nausea, watery diarrhea, and • If with pelvic
(TSST-1) marked hemoconcentration infections: requires
• Others: group A B-hemolytic • Complications: renal failure wound debridement
streptococcus serotypes M1 and M3, followed by hepatic failure, and possibly
Clostridium sordellii DIC and circulatory collapse hysterectomy
Source: CunninghamFG, el al. WilliamsObstetrics25th Edition;2018

176
THROMBOEMBOLIC DISEASE
I. ETIOPATHOGENESIS
A. Incidence
° Five times more common in pregnancy and puerperium
0 Early ambulation after delivery decreases the risk ofthromboembolic disease

B. Predisposing Factor:
0 Stasis
0 Oral contraceptive use before conception
0 Jobs where pregnant women sits for long period of time (sedentary lifestyle)
0 Deficiency of proteins involved in coagulation inhibition or in fibrinolytic system (e.g.,
Antithrombin-111, Protein-C, Protein-S, Plasminogen)

II. MANIFESTATIONS,
DIAGNOSIS,MANAGEMENT
MANIFESTATIONS I DIAGNOSIS I MANAGEMENT

■
Superficial Venous, Thrombo$is ·
• Thrombosis limited to the • Clinical • Analgesia
superficial veins of the saphenous • Elastic support
system
'!''i'1-
Deep Venq,us Thrombosis (DVT)
• Phlegmasia alba do lens or milk leg: • Compression • Anticoagulation
reflex arterial spasm causes a pale, ultrasonography throughout
cool extremity with diminished • D-dimer (if with low pregnancy and
pulsations probability of disease) postpartum
• Most are confined to the deep veins
of the lower extremity, leading to
pain, edema of the leg & thigh
Pulmonar,y Embolism-(PE)
• Causes 10% of maternal deaths • High index of suspicion • Anticoagulation
• May present with dyspnea, chest • Chest X-ray • Placement of
pain, syncope, hemoptysis • Ventilation/perfusion vena caval filters
• Massive PE: embolism causing scintigraphy considered
pulmonary instability with sudden • Computed tomographic • Thrombolysis
onset pulmonary hypertension and pulmonary angiography • Embolectomy
circulatory collapse
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018

Iii. ANTICOAGULATION
THERAPY
THERAPY I REMARKS
• Anticoagulation is initiated using either unfractionated heparin
(UFH) or Low molecular weight heparin (LMWH)
Heparin • UFH: initial treatment of thromboembolism and during delivery,
surgery or thrombolysis
• LMWH:preferred for acute venous thrombosis
• Vitamin K antagonist: contraindicated during pregnancy but can be
Warfarin
given orally during postpartum along with heparin
Newer oral • Dabigatran: thrombin inhibitor
anticoagulants • Rivaroxaban and apixaban: factor-Xa inhibitor

177
UTERINE COMPLICATIONS IN THE PUERPERIUM

ETlOPATHOGENESIS I MANIFESTATIONS I MANAGEMENT

Subinvolution
"
• Arrest or retardation of
involution
• Due to retained placental
fragments, pelvic infection
Postpartum Cervli:al Erosi/Jn/evePsion
• Cervical glands proliferate
occupying half of the entire
cervix
Relaxation of_Vagina{O~tlet and Prolapse of U.,terus,, ,.
• Extensive lacerations of
perineum during delivery
are followed by relaxation
of vaginal outlet
• Due to anatomic defects
of vaginal canal &
surrounding structures
• Umbilical cord traction
prior to placental
separation
• Uterus is larger and soft • Uterotonics (e.g.,
• Prolonged lochial discharge ergonovine,
• Irregular or excessive uterine methylergonovine)
bleeding or hemorrhage • Antibiotics
• Tissue appears red and • Cauterization or
velvety and may bleed even cryotherapy to remove
with the slightest touch persistent granulations
or the exposed
endocervical columnar
epithelium
• Pelvic heaviness, backache • Operative correction
• Mass protruding through • Manual repositioning
introitus of the uterus with
• Urinary tract problem anterior-posterior
• Vaginal bleeding/ discharge repair
• Vaginal hysterectomy
• Conservative: pessaries
and estrogen

178
DISORDERS OF THE BREAST
• Breast fever: not unusual for breasts to become distended with transient elevation of
temperature for the first 24 hours after commencement of lactation
• Puerperal fever from breast engorgement is common
• Fever seldom persists for> 16 hours

I. ABNORMALITIESOF SECRETION
• Marked individual variations in the amount of milk secreted
• It is not dependent on general health/ appearance of woman but on development of
glandular portion of breast:
0 Agalactia: no milk secretion
0 Polygalactia: excessive milk secretion
• Pituitary microadenoma: most common cause of galactorrhea, amenorrhea, estrogen
deficiency

II.OTHERS
I MANIFESTATIONS I MANAGEMENT
■
ETlOPATHOGENESIS

__ ____ =---------.------------'-~~-=....c..,~----~------"--------------1
1-B_r:~e~a"'s""C_'E_n"'g_o_11_y_e_m
e~n-t
• Due to exaggeration of normal • Pain • Support with brassiere
venous and lymphatic channels of • Transient increase • Cold compress
breast of temperature • Analgesic, antipyretic
• Breast pump/manual
expression of milk
Mastitis
• Infected breasts: parenchymatous • Chills or actual rigor, • Culture & sensitivity
infection of the mammary glands followed by fever & of milk
• Occurs on 3rd-4th week postpartum tachycardia • Antibiotics (penicillin /
(symptoms seldom occur in the first • Breast engorgement cephalosporin)
week postpartum) • Inflammation • Stop breastfeeding
• Infection is unilateral & marked temporarily
engorgement precedes inflammation • Drainage of abscess
• Staphylococcusaureus (most common)

• Due to clogging of a duct by • Pressure symptoms • May resolve

inspissated secretion, milk may spontaneously
accumulate • Aspiration
• Accumulation of milk in one or
more lobes of breast secondary to
clogging of duct by milk
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018

179
OTHER PROBLEMS IN THE PUERPERIUM
ETIOPATHOGENESIS
Maternityl'_Postpartum Blues
• Emotional letdown that
follows the excitement and
fears experienced during
pregnancy & delivery
• Common within the first week
postpartum
• Usually secondary to:
0 Discomforts of early
puerperium & delivery
° Fatigue from loss of sleep
0 Anxiety over capability to
care for the baby
,ii . •,;:
Neuromuscular &Join_tProblems
• Obstetrical neuropathies:
labor can cause pressure
on the branches of the
lumbosacral nerve plexus
• Musculoskeletal injuries:
stretching/tearing injuries
during normal or difficult
delivery
Urinary Retentio~f& Blaffder Qverdisteniion
• Antidiuretic effects of
oxytocin
• Local or conduction analgesia
may cause inability of bladder
to empty spontaneously
• Trauma to the bladder
(episiotomy, lacerations or
operative vaginal delivery)
I MANIFESTATIONS
"
• Emotionally labile
• Insomnia
• Weepiness
• Depression
• Anxiety
• Poor concentration
• Irritability
• Affective !ability
..
• Intense neuralgia and
cramp like pains
• If nerve is injured, pain,
sensory loss, & muscle
paralysis may ensue
• Median duration of
symptoms- 2months (2
weeks to 18 months)
• Enlarged bladder on
palpation
• Inability to void within 4
hours after delivery
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018
180
I MANAGEMENT
• Self-limited: 2-3 days
up to 10 days
• Effective treatment
includes anticipation,
recognition, and
reassurance
• May be improved
with counselling and
psychotherapies
·- "
~
.,
• Anti-inflammatory
• Physical therapy
• Examine for perinea!
and genital-tract
hematomas
• Insert indwelling foley
catheter for 24 hours,
until factors causing
retention have abated
• Intermittent self
catheterization
J. LEGALFRAMEWORKSRELATEDTO BREASTFEEDING
LEGAL
FRAMEWORK I REMARKS

Republic Act 7600: • An act providing incentives to all government and private health
Rooming-in and
institutions with rooming-in and breastfeeding practices for other
Breastfeeding Act
of1992 purposes

Republic Act 10028:

Expanded
• An act expanding the promotion of breastfeeding, amending for
Breastfeeding
the purpose Republic Act No. 7600

■
Promotion Act of
2009

• Immediate and thorough drying (within the first

Essential 30 seconds)
Intrapartum • Early skin-to-skin contact (after 3 seconds of
Newborn immediate drying)
Care (EINC) • Properly-timed cord clamping (1-3 minutes)
Protocol • Non-separation of newborn & mother for early
initiation of breastfeeding (within 90 mins of life)

Standards for
Rooming-in & • Rooming-inwithin 30 mins to 1 hour after delivery
Administrative
Order 2009-0025: Breastfeeding • Infants without complications shall be given to
Essential Newborn for Vaginal their mothers to hold and caress (skin-to-skin
Care Protocol deliveries contact) immediately after birth after the first
with awake 30 seconds of thorough drying
mothers

Standards • Let the mother hold and caress as soon as she

for Rooming- wakes up from the anesthesia, which can be
in and done in the recovery room
Breastfeeding
for Cesarean • Well infants are roomed-in within 3-4 hours
Section after birth
deliveries

• To protect & promote breastfeeding, the following are not allowed:

0 Advertising of breast-milk substitutes & other products
Executive Order 51: 0 Donation ofbreastmilk substitutes & supplies to maternity hospitals
Milk Code of the ° Free samples to mothers
Philippines 0 Promotion in the health centers
° Company personnel to advise mothers
0 Gifts or personal samples to health workers

181
 LEGAL
FRAMEWORK
I REMARKS

• Have a written breastfeeding policy that is routinely communicated

to all health care staff
• Train all health care staff in skills necessary to implement this policy
• Inform all pregnant women about the benefits and management of
breastfeeding
• Help mothers initiate breastfeeding within a half-hour of birth
Ten Steps to • Show mothers how to breastfeed, and how to maintain lactation
Successful even if they should be separated from their infants
Breastfeeding
• Give newborn infants no food or drink other than breast milk
(WHO/UNICEF
Statement 1989) unless medically indicated
• Practice rooming in: allow mothers and infants to remain together
(24 hours a day)
• Encourage breastfeeding on demand
• Give no artificial teats or pacifiers to breastfeeding infants
• Foster the establishment of breastfeeding support groups and refer
mothers to them on discharge from the hospital or clinic

World Health • To improve, through optimal feeding, the nutritional status, growth
Assembly and & development, health, and survival of infants & young children
UNICEF:Global • Supports exclusive breastfeeding for 6 months, followed by timely,
Strategy on Infant adequate, safe and appropriate complementary feeding, while
and Young Child continuing breastfeeding for two years and beyond.
Feeding in 2002 • Supports maternal nutrition, and social and community support

II. HUMANBREASTMILKCOMPOSITION
COMPONENT I AMOUNT
Fats
-
Total • 4.2 g/l00mL
Fatty acids • Trace
Polyunsaturated • 0.6 g/l00mL
fatty acids (PUFA)
Cholesterol • 0.016 g/1 00mL
Proteins
-
Total • 1.1 g/l00mL

Casein • 0.3 g/l00mL

A-Lactalbumin • 0.3 g/l00mL
Lactoferrin • 0.2 g/l00mL
Carbohydrates ll
Lactose • 7 g/l00mL
Oligosaccharides • 0.5 g/l00mL
Vitamins '-

VitaminK • Totally absent (thus Vitamin K is given IM to the newborn)

VitaminD • Low levels at 22 IU/mL, newborn supplementation necessary
Source:Cunningham
FG,et al. WilliamsObstetrics
25thEdition;2018

182
III. MILKPRODUCTIONSUPPLEMENT
• Malunggay capsule supplements can increase the breast milk quantity without affecting
its quality

Estrellaet al.,2000

IV. PROPER LATCHING

GOOD ATTACHMENT
• Baby's mouth is wide open
• The lower lip is turned out
• The chin is touching the
breast ( or nearly so)
• More areola is visible above
the baby's mouth than below
I POOR ATTACHMENT
• The mouth is not wide open
• The lower lip is pointing forward (it may also be turned in)
• The chin is away from the breast
• More areola is below the baby's mouth (you might see
equal amounts of areola above and below the mouth)
• The baby is sucking only on the nipple, which can
be painful for the mother. The baby cannot suckle

■
effectively or get the milk easily

V. BABY'SSUCKLING
GOOD SUCKLING I POOR SUCKLING
• The baby takes slow, deep sucks, • Rapid, shallow sucks and smacking or
sometimes pausing for a short time clicking sounds
• You can see or hear the baby swallowing • Has cheeks drawn in
• Baby's cheeks are full and not drawn • Feeds very frequently
inward during a feed • Feeds for a very long time - for more than an
• Baby finishes the feed & releases the hour at every feed
breast by him/herself & looks contented • Does not release breast & seems unsatisfied
• Mother feels no pain • Mother feels pain

VI. BREASTCARE
• Clean breasts with water only. Soaps, lotions, oils, and vaseline all interfere with the
natural lubrication of the skin
• Washing the breasts once a day as part of general body hygiene is sufficient
• It is not necessary to wash the breasts directly before feeds (this removes protective oils
and alters the scent that the baby can identify as his or her mother's breasts)
• Brassieres are not necessary, but can be used if desired

VII. CONTRAINDICATIONS TO BREASTFEEDING

• Use of street drugs/alcohol
• Infant with galactosemia
• Maternal infection (e.g., HIV,active PTB, varicella, herpes simplex)
• Use of neoplastic, thyroid, immunosuppressant drugs
• Undergoing treatment for breast cancer

VIII.ACCEPTABLE MEDICALINDICATIONSTO GIVEBREASTMILK

• Inborn error of metabolism (galactosemia, PKU, maple syrup urine disease)
• Very low birthweight (1,500 grams); <32 weeks AOG
• Infants at risk for potentially severe hypoglycemia (SGA,diabetic mothers)
• Mothers too ill postpartum to care for her baby
• Mothers taking medications contraindicated with breastfeeding

Source:WHO/UNICEF; 2009
CunninghamFG,et al. Williams
Obstetrics25thEdition;2018

183
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27. Schauberger CW, Rooney BL, Brimer LM: Factors that influence weight loss in the puerperium. Obstet Gynecol 79:424,
1992
28. Schimmer BP, Parker KL Contraception and pharmacotherapy of obstetrical and gynecological disorders. In Brunton LL,
Chabner BA, Knollmann BC (eds): Goodman and Gilman's The Pharmacological Basis of Therapeutics, 12th ed. New York.
McGraw-Hill, 2011
29. Stern JM, Kenner M, Herman TN, Reichlin S. Nursing behaviour, prolactin and postpartum amenorrhoea during prolonged
lactation in American and !Kung mothers. Clin Endocrine! (Oxf). I 986;25(3):247
30. Tapson VF: Acute pulmonary embolism. N Engl) Med 358:1037, 2008
31. Tuuli MG, Rampersad RM, Carbone JF, et al: Staples compared with subcuticular suture for skin closure after cesarean
delivery: a systematic review and meta-analysis. Obstet Gynecol 117(3):682, 2011
32. Tyson JE, Ito P, Guyda H, et al. Studies of prolactin secretion in human pregnancy. Am) Obstet Gynecol 1972; 113:14
33. WHO recommendations: uterotonics for the prevention of postpartum hemorrhage. Geneva: World Health Organization;
2018. License: CC BY-NY-SA
3.0 IGO
184
BLEEDING
DURING
PREGNANCY
AND
INPOSTPARTUM
 SECTION ONE
OVERVIEW OF BLEEDING DURING PREGNANCY
CAUSES OF BLEEDING DURING PREGNANCY
• Bleeding per vagina is common at ail stages of pregnancy
• Source of bleeding is almost always maternal, rather than fetal
DURING EARLY I DURING THE SECOND I POSTPARTUM
PREGNANCY HALF OF PREGNANCY HEMORRHAGE
• Abortion • Placenta previa • Uterine atony
• Ectopic pregnancy • Abruptio placenta • Retained placenta
• Cervical, vaginal, or • Morbidly adherent • Uterine rupture
uterine pathology (e.g., placenta (placenta accrete • Uterine inversion
infection, polyps) syndromes) • Genital tract trauma

I. EARLYPREGNANCYBLEEDING
• History of 2:2 early pregnancy losses or a condition associated with
History

Abdominal
early pregnancy loss (e.g., APAS)may suggest impending pregnancy loss
• Heavy bleeding, pelvic pain/cramping, passing of tissue may suggest
ectopic pregnancy or early pregnancy loss
• Midline pain: may suggest pregnancy loss
I
examination • Lateral pain: may suggest ectopic pregnancy
• To check for fetal heartbeat if pregnancy >10-12 weeks AOG
Doppler
• Doppler confirmation of fetal cardiac activity is reassuring, indicating
ultrasound
that bleeding is not related to fetal demise or ectopic pregnancy
External • Visual inspection and palpation to check for abnormalities (e.g.,
genitalia laceration, neoplasm, warts, polyps)
• Direct visualization of gestational sac in a dilated internal cervical os
Cervical os signifies that early pregnancy loss is inevitable
• A closed internal cervical os suggests a threatened early pregnancy loss
• There is no role for monitoring hCG concentrations once the presence of
an intrauterine pregnancy has been established sonographically
• Serial measurements are useful in the first 6 weeks of pregnancy if
~-hCG ultrasonography is non-diagnostic (i.e., location & viability of the
concentration pregnancy are not revealed)
• Failed pregnancy (i.e., nonviable intrauterine pregnancy): ~-hCG
levels plateau or fail
• Ectopic pregnancy: slowly rising hCG levels ( <35% over 48 hours)
Ultrasound • Cornerstone in the evaluation of bleeding in early pregnancy

II. BLEEDINGIN THE SECONDHALF OF PREGNANCY

• Digital examination of the cervix should be avoided in patients with bleeding in the
second half of pregnancy until placenta previa has been ruled out
• Transvaginal ultrasound is also the cornerstone in the evaluation, primarily to:
Determine whether the placenta is covering the cervical os (i.e., placenta previa)
Check for deciduai hemorrhage causing placental separation (i.e., abruptio placenta)
Check for cervical insufficiency (e.g., short length, dilated internal os)

Ill. POSTPARTUMHEMORRHAGE(PPH)
• PPH is an obstetric emergency
• Hemostasis normally occurs upon placental separation because uterine bleeding is
controlled by a combination of two mechanisms:
Contraction of the myometrium (which compresses the vessels)
• Local decidual hemostatic factors which cause clotting
187
 SECTION TWO
El,4\RLYPREGNANCY eOMPLICATIONS
OVERVIEW
• Vaginal bleeding is common in the first trimester
• The five major sources of nontraumatic bleeding in early pregnancy are:
Ectopic pregnancy
Early pregnancy loss
0

Implantation of the pregnancy

0

Abortion
° Cervical, vaginal, or uterine pathology (e.g., polyps, inflammation, infection)

ABORTION

I. NOMENCLATURE
TERM I DEFINITION
• Pregnancy termination or loss before 20 weeks of
Abortion
gestation or with a fetus delivered weighing <500 g
• May be threatened, inevitable, incomplete, complete or
Spontaneous abortion
missed abortion
Septic abortion • Abortion that is complicated by infection
• 2:3 early consecutive spontaneous abortions OR
Recurrent pregnancy loss
• 2:2 late consecutive spontaneous abortions
• Positive for ~-hCG testing but without a confirmed
Pregnancy of unknown sonographic location (gestational sac not yet sonological!y
location (PUL) visible transvaginally)
• ~-hCG<1500 mIU/mL
Source:POGSCPGonAbortion.2ndEdition.November
2015

II. PATHOGENESIS
• More than 80% of spontaneous abortions occur within the first 12 weeks of gestation
• Incidence increases significantly with advancing maternal age
• Most commonly presents with vaginal bleeding & suprapubic pain
• Hemorrhage into the decidua basalis & necrotic changes cause detachment of the embryo,
stimulating uterine contractions and expulsion

III. ETIOLOGY
FIRST TRIMESTER ABORTION I MIDTRIMESTER ABORTION
• Chromosomal anomaly (most common) • Cervical insufficiency
• Infections • Infections
• Medical disorders (e.g., thyroid disease, • Maternal uterine or cervical anatomic
DM,SLE,APAS) defects*
• Exposure to chemotherapy /radiation • Medical disorders
• Maternal uterine/cervical anatomic defects* • Exposure to fetotoxic agents
• Social and behavioral factors** • Trauma
• Paternal factors: increasing paternal age,
chromosomal abnormalities in spermatozoa
*Includesleiomyomata,
uterinesynechiae,cervicalincompetence
••HIV,uncomplicatedsurgicalprocedures,
dietarydeficiency
of anyonenutrientarenotassociated
withexcessive
abortionrisk.Traumaseldomcausesfirst-trimester
abortion.
"Heavy"caffeineconsumption
{morethan3 cupsper
day)coupledwithsmokingis associatedwithhigherriskof abortion.

188
A. Chromosomal Abnormalities
0 Responsible for most cases of early abortion (i.e., fetal factors)
0 Abnormalities in zygote development are the most common findings in early
spontaneous abortions

B. Cervical Insufficiency (Incompetent Cervix)

0 The cervix is dilated more than expected with the level of contractions experienced, or
painless cervical dilation & effacement in the 2nd trimester
0 Risk factors:
• History of cervical surgery (e.g. cone biopsy or dilation of the cervix)
• History of cervical lacerations with vaginal delivery
• Uterine anomalies
• History of diethylstillbestrol (DES) exposure

1. Management
TIMING I MANAGEMENT
If fetus previable • Expectant management
(<24 weeks) • Emergency cerclage

If with viable
pregnancies
•
•
•
•
Expectant management with strict bed rest
Steroid therapy*
Tocolysis during steroid therapy
Emergency cerclage
I
'Dependson cervicaldilatationand state of amnionicsac

2. Cercla2e
• Suture placed vaginally around the cervix either at the level of
the cervical-vaginal junction (McDonald) or at the internal os
(Shirodkar)
Emergency
• Goal is to close the cervix
cerclage
• Maintained until 36 - 38 weeks if possible
• Possible complications: rupture of membranes, preterm labor
(PTL), and infection
• Offered if with suspected cervical insufficiency in a previous
Elective cerclage at
pregnancy
12-14weeks
• Maintained until 36 - 38 weeks if possible

C. Antiphospholipid Antibody Syndrome (APAS)

0 Acquired antibodies targeted against a phospholipid, wherein pregnancy loss is
thought to involve placental thrombosis and infarction
0 Systemic autoimmune disorder characterized by venous or arterial thrombosis
and/or pregnancy morbidity in the presence of persistent laboratory evidence of
antiphospholipid antibodies (aPL)

189
III. CLINICAL CLASSIFICATION OF SPONTANEOUS ABORTION
TYPE
I DESCRIPTION I CERVIX I UTERUS• 1~·1 RiT< I PLAN
• Any bleeding
<20 weeks AOG,
without dilatation
of cervix or • Bed rest
Threatened
abortion
expulsion of Closed Compatible + + • Tocolysis
any products of
conception (i.e., a
normal pregnancy
with bleeding)

• Dead products
of conception • Cervical
Missed
abortion
that have been
retained for days
Closed Compatible + - ripening±
curettage'
or weeks

• Complete • Observe
expulsion of Incompatible • Measure
Complete
abortion
all products of
conception (POC)
Closed (small for
AOG)
- - hCG
• Trasvaginal
<20 weeks AOG ultrasound

• Partial expulsion
• Manage
(i.e., passage of
expectantly
meaty material) of Incompatible
Incomplete • Curettage•
abortion
some, but not all
POC <20 weeks
Open (small for
AOG)
- - • Prostaglandin
analog (e.g.,
• Part of placenta is
misoprostol•)
retained in uterus

• No expulsion
but with vaginal
bleeding & dilation
of the cervix such
• Expectant
that maintaining a
Inevitable • Oxytocin
abortion
viable pregnancy
is unlikely
Open Compatible - +/- • Curettage'
• There is rupture
of the membranes
in the presence of
cervical dilatation
• Uterus: compatible or incompatiblein relation to the age of gestation
'BOW: bag of water(+ would mean an intact BOW,i.e., not yet ruptured BOW)
'FHT: Fetal heart tone
'Await passage of fetus priorto curettage in late abortions (;?:12weeksAOG)
• Misoprostolis not approved for use in the local setting

190
IV.OTHERTYPES OF ABORTION
TYPE I DESCRIPTION
• ;?3 early consecutive spontaneous abortions or
Recurrent
;?2 late consecutive spontaneous abortions
pregnancy loss
(RPL) • Work-up for anatomic, metabolic immunologic, genetic, and infectious
causes
• Abortion with infection of the products of conception (POC), uterus,
and adnexa
• Usually polymicrobial
• Diagnosis of septic abortion:
0 Temperature ;?38°Cof at least 24-hrs duration & unattributable to
Septic abortion
any other cause
0 History of mechanical instrumentation for the purpose of inducing
an abortion
0 Presence of septic discharge from the cervix
Tenderness of the uterus, parametrium or adnexa

I
0

• Induced abortion, done for whatever reason, is considered illegal in

the Philippines:
Induced 0 Therapeutic abortion: done with medical indications for the sake of · -
abortion the mother's health ;"
0 Elective abortion (voluntary abortion): done upon the request of
the woman with no medical or obstetric indications

V. DIAGNOSIS
DIAGNOSTICS I REMARKS
• Urine or serum 8-hCG
Basic tests • CBC,blood typing
• Transvaginal ultrasound
• Sonographic findings in early pregnancy loss:
° Crown-rump length (CRL) ;?7 mm and no heartbeat
0 Mean gestational sac diameter (MSD) ;?25 mm and no embryo
0 An initial ultrasound shows gestational sac with yolk sac, and
Ultrasound
after "11 days
no embryo with heartbeat is seen
0 An initial ultrasound shows a GSwithout yolk sac, and after <:2weeks
no embryo with a heartbeat is seen

VI. MANAGEMENTOF MISSEDAND INCOMPLETEABORTION

AGE OF
GESTATION

• Missed abortion: dilation & curettage

<12weeks • Incomplete abortion: completion curettage
• Curettage may be done at any time
• Missed abortion: dilation & evacuation/ extraction
• Prostaglandin • Incomplete abortion: completion curettage
11
• Ergot alkaloids • Curettage may be done after passage of fetus as
• Oxytocin confirmed on ultrasound
~12weeks 0 At this AOG,fetus already has bony spicules,
which may cause lacerations and perforations
to the uterine, cervical, and/ or vaginal wall
during curettage

191
ECTOPIC PREGNANCY
• Implantation of the fertilized ovum outside the endometrial lining of the uterine cavity
• May implant in the fallopian tube, ovary, cervix, abdomen (normal: should be intrauterine)
• All women with early pregnancy bleeding and pain are assumed to have ectopic
pregnancy until excluded by laboratory and sonography

I. ETIOPATHOGENESIS
A. Risk Factors
0 Prior ectopic pregnancy (strongest risk factor)
0 Previous tubal surgery
0 Smoking >20 cigarettes per day
0 PID confirmed by laparoscopy or positive test for Chlamydia trachomatis
0 ;;,3 prior miscarriages
0 Age e,40 years old
0 Prior abortion (medical or surgical
0 Infertility >l year
0 Lifelong sexual partners > 5
0 Prior IUD use

• Pregnancy along the length of the fallopain tube

Tubal • Possible locations: ampulla (70%). isthmus (12%), fimbria (11 %) and
Pregnancy interstitium (2%) tubal portions
(most • Transit of fertilized ovum is blocked, causing it to implant in the fallopian tube
common} • Expectant vs medical (methotrexate) vs surgical (salpigostomy/segmental
resection or complete salpingectomy)
• Pregnancy within the proximal intramural portion of the fallopian tube
• Sometimes incorrectly labeled as cornual pregnancy
Interstitial
• Management:
pregnancy 0Medical (methotrexate)
0Surgical (wedge resection or hysterectomy)
Heterotopic • Simultaneous ectopic+ intrauterine pregnancies
Pregnancy • Removal of the ectopic pregnancy
• Pregnancy implanted within the endocervix at or below the cervical os
Cervical • Management:
Pregnancy 0Medical (methotrexate)
0Surgical (hysterectomy)
• Satisfies the Spiegelberg Criteria
0The tube on the ipsilateral side is intact
Ovarian 0The ectopic pregnancy occupies the ovary
Pregnancy 0The ectopicpregnancy is attached to the uterus by the utero-ovarianligament
0Ovarian tissue is identified histologically amid placental tissue
• Ovarian wedge resection/oophorectomy

• A pregnancy wherein the blastocyst implants on scar tissues within the

Cesarean myometrial defect of a previous cesarean surgery.
Scar • Management:
Pregnancy 0Medical (methotrexate)
0Surgical (hysterectomy)
• A pregnancy in the peritoneal cavity exclusive of tubal, ovarian, or
intraligamentary implantations.
• Management depends on AOG at diagnosis and placental implantation
Abdominal 0 Non-viable pregnancies are managed medically or surgically
Pregnancy 0 Viable pregnancies are watchfully brought close to term and delivered

abdominally for maternal or fetal indications (placenta usually left in

place to prevent hemorrhage on detachment and resorbed medically with
methotrexate)
ource:
192
 C. Various Sites and Frequency of Ectopic Pregnancies
Interstitial (2-3%)

lsthmic (12%)

Tubal
(95-96%)

Ampullary (70%)

Fimbrial (11%)

Ovarian(3%)

Caesarean scar (<1%)

Cervical (<1%)
-----------------------< Non-tubal
(4-5%)

L------==----------------A-b-do_•~_
0
_i~_:_~~_l:_y~-)
________ ..J ■
Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018

II. MANIFESTATIONS
• Classic triad of symptoms:
Amenorrhea
0
Symptoms
Abdominal pain (95%)
0

Vaginal bleeding/spotting
0 (60-80%)
• Uterus may be slightly enlarged and pushed to one side
• Vital signs: normal (unruptured) or hypotension (ruptured)
• Adnexal mass that is often tender
Signs
• Small corpus compared to AOG
• Cervical motion tenderness
• Bulging of posterior vaginal fornix (accumulation of blood in cul-de-sac)

A. Differential Diagnoses of Ectopic Pregnancy

Abortion
0

° Corpus luteum cyst

° Cystic ovarian masses
Appendicitis (due to exquisite pain especially when pain is on the right lower quadrant)
0

Pelvic inflammatory disease (pain and wiggling tenderness)

0

B. Ruptured Ectopic Pregnancy

Ruptured ectopic pregnancy may present with hypotension, tachycardia, or signs of
0

peritoneal irritation secondary to hemoperitoneum

Usually ruptures >8 weeks due to the maximal distention of the muscularis
0

Presents with severe hemorrhage due to close proximity to uterine & ovarian arteries
0

Management
0

• Requires emergency exploratory laparotomy or laparoscopy

• Blood transfusion if hemodynamically unstable
• Salpingectomy

193
III. DIAGNOSIS
DIAGNOSTICS I REMARKS
• Findings in ectopic pregnancy: P-hCG Levels are lower than those in
normal intrauterine pregnancies
• Normal rate of increase in P-hCG Levels or "doubling time" does not
fl-hCG: urine or occur in ectopic pregnancy
serum • Intrauterine pregnancy not seen on transvaginal ultrasound after
attaining discriminatory serum P-hCGlevel ofeel,500 mlU/mL
• Fetal heartbeat, whether intrauterine or ectopic should be seen on
transvaginal ultrasound at P-hCGlevels ee5,000 mlU/mL
• Should be 10-25 ng/mL
Serum
• Levels are lower compared to normal gestation
progesterone
• There is no viable pregnancy if serum progesterone is <0.5 ng/mL
• Presence of
° Complex adnexal mass separate from the ovary and fluid in cul-de-sac
0Pseudogestational sac/pseudosac: fluid collection that is seen in the
midline within the endometrial cavity
• In contrast, gestational sac of normal pregnancy (seen between
4-5 weeks AOG)implants eccentrically within the endometrial cavity
Ultrasound
and has the double decidual sac sign
• Absence of an intrauterine gestational sac on transvaginal ultrasound
(TVS) when the ~-hCGlevel is eel,500 mlU/mL
• Presence of an intrauterine gestational sac rules out an ectopic
pregnancy, except in a heterotopic pregnancy (an ectopic pregnancy
occurs at the same time as a normal intrauterine pregnancy)
I
• Aspiration of non-clotting blood from cul-de-sac through the posterior
vaginal fornix is indicative ofhemoperitoneum
• Hemoperitoneum is extravasated blood that has clotted & lysed
Culdocentesis • False negative interpretations may be due to:
Blood aspirated from pelvic vessels (clotting blood}, or
0 •

Hemopertoneium is still clotted (i.e., no blood aspirated)

0

• No longer done with the advent oftransvaginal ultrasound

• Gold standard in the diagnosis of ectopic pregnancies
• Direct visualization of the pelvic organs would be possible
• Done only in hemodynamically stable patients
Laparoscopy • Diagnosis cannot be confirmed in presence of massive hemoperitoneum
• May proceed with operative laparoscopy once diagnosis confirmed
0 Better results (shorter hospitalization, less blood loss)
0 Improved prognosis (less post-op adhesions)

IV.MANAGEMENT
A. Expectant Management
0 Observing the ectopic pregnancy to resolve naturally without intervention
0 Recommended ~-hCG monitoring is every 48 hours (three consecutive decreasing
measurements is reassuring)

Criteria for Exoectant Mana_qement in Ectopic Pre_qnancv:

Done when risk of tubal rupture is minimal:
• Hemodynamically stable and minimal abdominal pain
• Initial p-hCG <1000 IU/L
• No gestational sac or extra uterine mass suspicious for an ectopic pregnancy
Expectant management is contraindicated if:
• With significant increase in abdominal pain, or
• Serum P-hCG increases or fails to decrease (decrease of>10% across two consecutive
measurements)
Source:POGSCPGon EctopicPregnancy,
Nov2016.
194
B. Methotrexate (MTX)
It is a folic acid antagonist: binds to dihydrofolate reductase which reduces
0

dihydrofolate to tetrahydrofolate (active form of folic acid), leading to arrest in DNA,

RNA and protein synthesis of rapidly proliferating tissue such as trophoblasts
Side effects: stomatitis, GI symptoms, bone marrow suppression
0

1. Indications and Contraindications to Methotrexate

INDICATIONS I CONTRAINDICATIONS

• Pregnancy is <6 weeks • Active bleeding

• Asymptomatic • Breastfeeding
• Hemodynamically stable patient • Immunodeficiency
• Compliant to follow-up and medication • Alcoholism
• Low initial p-hCG • Blood dyscrasia
(usually <5,000 mIU/mL) • Liver or renal disease
• Small ectopic pregnancy size ( <3.5 cm) • Active pulmonary disease
• No cardiac activity • Sensitivity to MTX
• Tubal rupture
• Intrauterine pregnancy
• Peptic ulcer disease

2. Dose ofMethotrexate

Dosing
I SINGLE DOSE

• One dose
I MULTIDOSE

• Up to 4 doses until serum B-hCG

■
• Repeat if necessary decreases by 15%
• 50 mg/m' body surface area
MTX • 1 mg/kg days 1, 3, 5, 7
(BSA) (day 1)
Leucovorin • NA • 0.1 mg/kg days 2, 4, 6, 8
Serumf3-hCG
• Day 1 (baseline), 4, and 7 • Days 1 (baseline), 3, 5, and 7
monitoring
• B-hCG does not decrease by • B-hCG decreases by <15%
Indications 15% from day 4 to 7 • Repeat B-hCG in 48 hrs &
for additional
• Less than 15% l during compare with previous value
dose
weekly surveillance • Maximum: 4 doses
• Once 15% reduction achieved, do weekly P-hCG determination
until it becomes undetectable
• Indications for surgical intervention
Surveillance 0 Decrease in B-hCG continues to be less than optimum
0 Increase in B-hCG

0 Rupture of ectopic pregnancy and patient becomes symptomatic

C. Surgical Management*
• Used to remove unruptured pregnancy that is <2 cm in size
• 10- to 15-mm linear incision is made at the antimesenteric border;
Saipingostomy products of conception is flushed out
• Incision is not sutured and left to heal via secondary intention
• Hemostatic control is done by bipolar cauterization
• Same as salpingostomy, except that the incision is closed with
delayed-absorbable suture
Salpingotomy
• No longer done because of more tubal scarring and adhesion
formation observed
Salpingectomy • Complete excision of the fallopian tube
'Laparoscopicsurgeryis preferredunlesspatientis hemodynamically
unstable(versuslaparotomy)

195
ABORTION VERSUS ECTOPIC PREGNANCY

I ABORTION I ECTOPIC PREGNANCY

,_Manifestations ,,__ -
-
Amenorrhea • Present • Present
• Spotting to profuse (threatened
Bleeding • Spotting
to incomplete abortion)
• Pelvic pain depending on laterality
(localized peritoneal irritation at
• Hypogastrium (because pain the area of the ectopic pregnancy)
Pain is due to contractions of the • Abdomen, neck or shoulder
uterus in the midline) (hemoperitoneum from ruptured
ectopic pregnancy causes
diaphragmatic irritation)
• Stable • Stable if not ruptured
Vital signs • Unstable:ifwith severe hemorrhage, • Unstable: if with severe hemorrhage,
hypovolemia, or septic shock hypovolemia, or septic shock
• Tender
• Non-tender • Signs of peritonitis if ruptured, due
Abdomen • Tender if with uterine to hemoperitoneum
contractions • Classic triad: amenorrhea, vaginal
bleeding, and abdominal pain
• Closed: threatened, missed, or • Closed, tender
Cervix complete • Cervical motion tenderness due to
• Open: incomplete or inevitable peritonitis
• Compatible for dates:
threatened, inevitable • Small (conceptus is not within uterine
Corpus
• Small for AOG:incomplete, cavity so it will not be enlarged
complete, or missed
Adnexa
D.{ag[losis •
11.
• (-)mass/tenderness

..~11~-
_.,
,.
. ~
.
• ( +) mass/tenderness
~
,,
~ ".ii''-'
Serum
• <5 ng/mL • <25 ng/ml
progesterone
• Insufficient to maintain the • Does not reach the normal pregnant
(normal is
225ng/ml) pregnancy levels

• Impaired doubling time

Serial B-hCG
• No normal production of ~-hCG
• Absent gestational sac (GS)
Transvaginal • Intrauterine gestational sac
UTZ· • Adnexal mass (i.e., GS may be seen
(GS)
at adnexa)
• Empty uterus
• Abnormal intrauterine
Sonography pregnancy (IUP)
• ( +/-) adnexal mass
and • At ~-hCG >1500 mlU/mL, an
• ~-hCGwould depend on AOG,
Quantitative intrauterine GSshould be visualized
SerumB-hCG but a decreasing trend points to
(if none, consider a possible ectopic
a failing pregnancy
pregnancy)
Uterine
• Villi are present • No villi
Curettage
Laparoscopy • Not indicated • For stable/unruptured cases
Laparotomy • Not indicated • For unstable/ ruptured cases

196
 SECTION THREE
'

BLEEDING IN THE SECOND HALF OF PREGNANCY

OVERVIEW OF BLEEDING IN THE SECOND HALF OF PREGNANCY

I. ANTEPARTUMHEMORRHAGE
• Vaginal bleeding from the genital tract during the 24th week of pregnancy and prior to
childbirth
• Most important causes of APH are placenta previa and placental abruption
,,,
Obste1r-fc causes
• Placental abruption, placenta previa
Placental • Vasa previa (patient bleeds from a blood vessel located on the amniotic
membranes of placenta)
Maternal • Uterine rupture
Fetal • Fetal vessel rupture

■
-:-<
Non-obstetric causes
Cervical • Severe cervicitis, polyps, cervical dysplasia/cancer
Vaginal/vulvar . • Lacerations, varices, cancer
Other • Hemorrhoids, bleeding disorder, trauma, hematuria
Source:HackerN, et al. Essentialsof ObstetricsandGynecology.
Philadelphia, PA:WBSaunders;1992:155.

II. PLACENTAPREVIAVERSUSABRUPTIOPLACENTA
I PLACENTA PREVlA I ABRUPTIO PLACENTA
• Placenta abnormally implanted • Premature separation of a
in the lower uterine segment normally implanted placenta prior
or lower uterine segment (LUS) to delivery
Definition
(passive segment)
• Internal os covered partially or
completely by the placenta

Illustration

197
 I PLACENTA PREVIA I ABRUPTIO PLACENTA
Clinical 11.ist_ory
Hemorrhages • Profuse bleeding • Single episode
Abdominal Pain* • Absent • Common
Physical Examinat1o_n . -

• Local uterine tenderness

• Normal uterine tone
Uterus • Hypertonic / tetanic "woody"
• Non-tender uterus
uterus
Labor • Patient rarely in labor • Patient usually in labor
Engagement • Presenting part unengaged • Presenting part often engaged
Fetal Parts • Palpable abdominally • Difficult to palpate abdominally
Fetal Heart Tones • Auscultated easily • Auscultated with difficulty
Ancillary Aids & Other Examinatio,t's
• Placenta in lower uterine segment
Ultrasound • Placental detachment
• Placenta covering internal os
Vaginal • No placenta within 5 cm of
Examination • Palpable placental cotyledons internal os
(under double at the cervical os • Bloody amnionic fluid on
set-up) amniotomy is pathognomonic
• No place for expectant treatment
• Tocolysis or expectant when diagnosis is made
management is done if bleeding • Emergency CS for fetal distress
stops & fetus is <36 weeks AOG and/or incessant bleeding
Management
• Emergency cesarean section • If with intrauterine fetal
(CS) for fetal distress and/or demise, induction of labor
incessant vaginal bleeding should be done and vaginal
delivery usually ensues
•commonteachingis "PAINFUL uterinebleeding:abruptioplacenta.PAINLESS
uterinebleeding:placentaprevia'.
Thisis notalwaystrue,as laboraccompanying placentapreviamaycause pain. Painforabruptioplacentamay
mimicnormallabor)
Source:OxornH.et al.Appleton& Lange;1986

198
PLACENTA PREVIA
• Normally, the placenta is implanted near or at the fund us of the uterus (which is part of
the active segment)
• Placenta previa means placenta goes first before fetus in the birth canal ("Previa" means
"going before")
• Condition wherein the placenta is abnormally implanted in the lower uterine segment
(passive segment), either over or near the internal cervical os

I. ETIOPATHOGENESIS
A. Classification of Placenta Previa

• Total placenta previa

0 Internal os is completely covered by
placenta
Placeta
previa • Partial Placenta Previa
(Placenta Previa Partialis)
0 The internal os is covered partially
by placenta I
Total Partial
placenta previa placenta previa

• Marginal Placenta Previa

(Placenta Previa Marginalis)
0 Edge of the placenta at the margin of
Low- internal os
lying 0 Implantation in the lower uterine
placenta segment wherein the placental edge
does not cover the internal os but
lies within the 2-cm wide perimeter
around the os
Marginal
placenta previa
B. Pathophysiology: Mechanism of Bleeding
Placental implantation in the LUS
0

Defective decidual vascularization

0

Disruption of placental attachment in the LUS(3rd trimester)

0

Thrombin release from the bleeding sites

0

Promotes uterine contractions

0

Placental separation and bleeding

0

C. Risk Factors
• Maternal age (>35 years old) • Low socioeconomic status
• Multiparity • Short interpregnancy interval
• Prior uterine surgery (e.g., CS) • Cocaine use
• Recurrent abortions • Abnormally elevated maternal serum
• Smoking alpha-fetoprotein (MSAFP)levels
• Uterine leiomyoma • Infertility treatment/assisted
• Multiple gestation reproductive technology (ART)
• Erythroblastosis • Others (e.g., digital exam, abruptio
• Non-white ethnicity placenta, trauma)

199
II. MANIFESTATIONS
• Suspected in any woman >20 weeks AOGwith painless vaginal
bleeding (classic presentation) usually near the end of the second
trimester
Symptoms
• Repeated "warning" hemorrhages ("sentinel bleed")
• Absent abdominal pain ("painless vaginal bleeding")
• Not associated with toxemia (in contrast to abruptio placenta)
• Normal uterine ton~ & non-tender
• Patient rarely in labor
• Presenting part is unengaged (in 35% of cases: non-cephalic presentation)
Signs
• Fetal parts are usually palpable abdominally
• Fetal heart tones usually present on abdominal auscultation
• Internal examination is contraindicated

III. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Speculum examination may be done gently
• Internal examination is contraindicated in cases of placenta previa
Vaginal • If unknown placental location in patients clinically suspected with
examination placenta previa, internal examination can be done in a double set-up
(i.e., performed in the operating room prepared for an emergency CS
delivery)
• Can already make a diagnosis (even the type of placenta previa)
Ultrasound
• Placenta is seen in the LUS
Basic • CBC,blood typing, PT/PTT
laboratory • Fibrinogen, D-dimer if suspecting disseminated intravascular
work-up coagulation (DIC)

IV.MANAGEMENT
Initial • Secure IV access and blood products
stabilization • Continuous fetal monitoring
• Steroid therapy for fetal lung maturity.
Prepare for
• Magnesium sulfate (between 24-32 weeks) for neuroprotection if
preterm
delivery is occurring within 24 hours
delivery
• Cautious use of tocolytics as long as mother and fetus are stable
• Depends of final placental localization (usually determined between
32-36 weeks)
• Vaginal delivery:
0If placental edge >2 cm away from os: trial of labor
0If placental edge within 0-20 mm from os: vaginal delivery is still
Route of possible, but proceed with caution
delivery • Cesarean section (delivery of choice):
° For all women with placenta previa
° For near term and with no bleeding, schedule elective CS at term
[usually 38 weeks)
0Midline vertical laporotomy incision: recommended for rapid entry in
case of bleeding or in case hysterectomy is needed
Indications
• Active labor
for immediate
• Fetal distress
CS regardless
ofAOG • Life-threatening hemorrhage

200
ABRUPTIO PLACENTA
• Premature separation of normally implanted placenta before birth of a viable fetus

I. ETIOPATHOGENESIS
• Premature separation of a normally implanted placenta
• Diagnosis is typically reserved for pregnancies over 20 weeks of gestation

A. Classification of Placenta Previa

CLASSIFICATION REMARKS

0nset of Manifestations
Acute abruptio • Sudden onset of signs and symptoms
• Shows non-expanding or shrinking retroplacental hematoma
formation on serial ultrasound
• Chronic abruption-oligohydramnios sequence (CAOS):
Chronic abruptio ° Chronic abruption severe enough to result to oligohydramnios
0 Mean AOG at delivery: 28 weeks
° Continuous fetal heart rate monitoring does not universally

Severity

Mild abruptio
guarantee good fetal outcomes

• Partial abruption
- - I
• Mother and fetus are undisturbed
• Maternal tachycardia with orthostatic hypotension
Moderate abruptio
• Fetal distress
• Maternal shock
Severe abruptio
• Fetal demise

B. Types Based on Extent of Separation

PARTIAL SEPARATION I TOTAL (COMPLETE) SEPARATION

• Separation of the placenta is incomplete • Separation of the placenta is complete

(i.e., placenta does not completely detach (i.e., placenta completely detaches from
from uterine wall) uterine wall)

Partial
separation

201
C. Types Based on Mode of Bleeding
TYPE I REMARKS I ILLUSTRATION

• Bleeding passes between membranes

and uterine walls and escapes (or
drains) through the cervix, causing
External
apparent vaginal bleeding
• Better prognosis by earlier detection Blood leaks
and timely intervention through the
vagina

• Bleeding is not seen externally (i.e.,

retained between the detached
placenta and the uterine wall
• May extravasate into amniotic cavity
after breaking through the membrane
Blood is
(resulting in the pathognomonic
retained
Concealed bloody amniotic fluid)
inside the
• Bleeding may accumulate causing
uterus
increased pressure within the
concealed space and further
detachment of the placenta
• May lead to poorer prognosis due to
delayed detection and intervention
Marginal • By virtue of location and easy access of bleeding externally, placental
Sinus separation is limited to the margins with minimal bleeding without
Rupture uterine tenderness and pain

D. Pathophysiology
• Likely begins with rupture of a decidual spiral arteries resulting in an expanding
retroplacental hematoma
• Extravasation into the decidua basalis causing the decidua to split, leaving a thin layer
adhered to the myometrium
• This leads to decidual hematoma and expands to cause separation and compression of
the adjacent placenta
•Maybe due to acute process from one of the following:
• Uncontrolled hypertension
• Shearing forces resulting from trauma
• Sudden uterine decompression from membrane rupture associated with hydramnios
• Cocaine usage leading to acute vasoconstriction with resultant placental separation

E. Risk Factors
• Increased age and parity • Single umbilical artery
• Race • Multifetal gestation
• Pregnancy-induced hypertension • Low fetal weight
(most common associated condition) • Uterine leiomyoma (especially if located
• Prior abruption near the mucosa! surface behind the
• Hydramnios placental implantation site)
• Preterm ruptured membranes • Cigarette smoking
• Chorioamnionitis • Cocaine use

202
II. MANIFESTATIONS
A. Clinical Manifestations
• Most common presentation: sudden-onset abdominal pain, vaginal
Symptoms bleeding, and uterine tenderness
• Abdominal pain, uterine tenderness or back pain
• Vaginal bleeding >20 weeks AOG
• Hypertonic/tetanic "woody" uterus
• Frequently associated with hypertension
• Patient usually in labor
Signs
• Presenting part often engaged
• Fetal parts may be difficult to palpate
• Fetal heart tones may be difficult to detect (due to tetanic uterus) or
absent (i.e., dead fetus)

B. Manifestations based on Severity

I MILD
I MODERATE
I SEVERE
• Stable

I
• Elevated pulse rate
• Minimal
Mother • Hypotension • Shock/unstable
manifestations
• Reduced CVP
• Normal CVP
• Normal (reassuring) • Alive but+/- signs • Fetal distress
Fetus
FHT of fetal distress • Fetal death
• None • None
• Renal failure
Complications • Good urine output • Marginal urine
• Coagulopathy
• No clotting problems output
• Irritable • Severe pain &
• Irritable
Uterus • More pain tenderness
• Pain tenderness
• Severe tenderness • Tetanic contractions
• <500 mL
Bleeding • 500-1000 mL • >1000 mL
• No active bleeding
Placental
• < 1/6 • 1/6 to 2/3 • >2/3
Separation

C. Differentials
0Placenta previa
0Appendicitis
0Preterm labor
° Fibroid degeneration
0Ovarian pathology
0Muscular pain
'UT!

D. Complications
0Perinatal mortality
0Acute renal failure
0Hypovolemia/hemorrhagic shock
0Uterine atony
° Couvelaire uterus (uteroplacental apoplexy)
0DIC (abruptio placenta is most common etiology)

203
III. DIAGNOSIS
Vaginal • Done under double set-up if unsure of placental location
examination • Findings: no placenta within S cm of internal os
• Placenta seen in the upper uterine segment (UUS)with retroplacental
Ultrasound
clot/hematoma
• Recurrent late or variable decelerations
• Reduced variability, bradycardia or a sinusoidal pattern
EFMtesting
• Often associated with observed increased baseline uterine tone on
tocomonitoring
• Put sample of blood in a test tube
Clot
• Coagulation defect is positive if:
observation
test ° Clot does not form within 6 mins, or
° Forms and lyses within 30 mins

IV:MANAGEMENT
A. Overview of Management
• Stabilize the patient
• Prepare for the possibility of hemorrhage to worsen
Initial
• Prepare for delivery (if preterm, give steroids, magnesium sulfate as
management
indicated)
• Deliver if bleeding is life-threatening or fetal testing is non-reassuring
• Amniotomy (both diagnos!ic and therapeutic)
° Confirms diagnosis with observed bloody amniotic fluid
0 Prevents further placental separation with the baby having a
tamponade effect on the retroplacental hematoma
0 Prevents further release of thromboplastins into the circulation
• Vaginal delivery:
0 Both maternal and fetal status are stable, consider induction with
Term/
close monitoring
near term
° Cervix almost fully dilated
° Fetus is dead but mother is stable
• Cesarean Section (CS):
0 There is fetal compromise
• Severe uterine hypertonus
0 Life-threatening vaginal bleeding or DIC,or
0 Vaginal delivery is not imminent

B. Management Depends on the AOGand Fetomaternal Status

Stable • <34 weeks: expectant management
maternal and • 34-36 weeks: may do expectant management but with close monitoring
fetal status • 2'36 weeks: deliver
• Expeditious delivery
Unstable
• Prompt CS if:
mother and/ 0 Mother is unstable or FHR pattern is non-reassuring, AND
or fetus at
anyAOG
0 Vaginal delivery is not imminent, contraindicated (e.g., prior classical
CS,malpresentation), or unsuccessful (failure to progress)
• Vaginal delivery is preferable
• CSis often the best option when:
For fetal
demise
0 Rapid control of bleeding is required and delivery is not imminent
0With obstetric contraindications to vaginal birth, or
0 Mother is unwilling to accept adequate blood replacement therapy
Source:POGSCPGon Obstetric
Hemorrhage,
2014

204
MORBIDLY ADHERENT PLACENTA (ACCRETE SYNDROMES)
I. ETIOPATHOGENESIS
• Abnormally adherent villi to the myometrium:
• Partial or total absence of the decidua basalis or
• Imperfect development of the fibrinoid or Nitabuch layer
• Microscopically, placental villi are anchored to muscle fibers rather than to decidual cells
• Normally, cytotrophoblasts should control decidual invasion through factors such as
angiogenesis and growth expression

TYPE I DESCRIPTION

• Villiare attached to
Accreta*
the myometrium

Increta • Villi invade the

1-------t--m-yo_m_e_m_·u_m __ ---1
I
-
;:

• Villi penetrate
through the
Percreta
myometrium to or
through the serosa

'Typesof placenta
accreta
• Totalaccreta:abnormal adherence mayinvolveall lobules
• Focalaccreta:all or partof a lobuleis abnormally
attached

B. Risk Factors
• Prior cesarean delivery (especially if done as emergency CS)
• Risk factors associated with placenta previa (see previous section on Placenta Previa)
• Maternal serum: MSAFPlevels >2.5 Multiples of the Median or MoM (Bx) or
B-hCGlevels >2.5 MoM (4x)
• Prior myomectomy or reconstructive surgery
• Asherman syndrome
• Submucous leiomyomata
• Multiparity (>G6)

II. MANIFESTATIONS
AND DIAGNOSIS
• In some with no associated previa, accreta may not be identified until the 3rd stage labor
• Diagnosed via ultrasound with Doppler studies:
Loss of hypoechoic retroplacental zone, which correspond to the decidua basalis,
myometrium, and dilated venous channels
Progressive thinning of the retroplacental hypoechoic zone to <2 mm on serial exams
Placental vascular lacunae or "lakes" which represent dilated vessels extending from
the placenta through the myometrium having a "Swiss cheese" appearance (placenta
increta/placenta percreta)
Thinning/focal disruption of uterine serosa-bladder wall complex (placenta percreta)
Focal mass-like elevation with the same echogenicity as the placenta beyond the
uterine serosa (placenta percreta)

205
III. MANAGEMENT
A. Criteria for Consideration of Delivery in an Accrete Center of Excellence
• Suspicion for morbidly adherent placenta on ultrasound
• Placenta previa with abnormal ultrasound appearance
• Placenta previa with >3 prior cesarean deliveries
• Prior CS delivery and anterior placentation
• Prior endometrial ablation or pelvic irradiation
• Inability to adequately evaluate or exclude placenta accrete
• Suspicion of morbidly adherent placenta
Source:Silver,et al. 2015
CunninghamFG,et al. WilliamsObstetrics25thEd;2018

B. Other Aspects in Management

• Give corticosteroids for pregnancies between 24-36 weeks AOG at risk
of delivery within 7 days
General
• May give MgSO, between 24-32 weeks AOG for neuroprotection if
delivery is occurring within 24 hrs
• If with significant bleeding: possible CS hysterectomy regardless of AOG
• If asymptomatic: do elective CS hysterectomy at 36-37 weeks after
giving corticosteroid
Delivery
• After fetal delivery, extent of placental invasion is assessed without
attempts at manual placental removal
• Hysterectomy is performed with the placenta still in place
• Cases in whom accreta was not suspected before CS:
Conservative 0 Repair of hysterotomy done with placenta left in-situ
management 0 Administer methotrexate
in select
cases
0 When hysterectomy is necessary, transfer to a higher-level facility for
interval (delayed) hysterectomy to improve surgical risk
Source:POGSCPGon ObstetricHemorrhage,2014

206
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
I. ETIOPATHOGENESIS
• DICis a syndrome characterized by:
Widespread systemic activation of coagulation
Thrombotic obstruction of small and midsize vessels, eventually causing tissue
0

ischemia and bleeding from consumption of platelets and coagulation factors

A. Pathogenesis
DICis a systemic thrombohemorrhagic disorder seen in association with well-defined
clinical situations and laboratory evidence of:
• Procoagulant activation
• Fibrinolytic activation
• Inhibitor consumption
• Biochemical evidence of end-organ damage or failure
• Associated with septic abortion and chorioamnionitis
Intrinsic • Damage of the vessel wall and subsequent exposure of collagen
pathway
activates factors XII initiating the coagulation cascade
(Endothelial
damage) • Slow process, since circulating coagulation factors which are inactive
are subsequently activated

■
Extrinsic • Associated with abruptio placenta, amniotic fluid embolism, retained
pathway dead fetus, saline-induced abortion
(Massive • Rapid process, wherein procoagulant materials from tissue injury are
tissue injury) not usually present in the blood stream

B. Etiology /Risk Factors

Pregnancy
0

Abruptio placenta (most common obstetric cause of DIC)

0

Preeclampsia/eclampsia
0

Intrauterine fetal demise (>l month)

0

Septic abortion or obstetric sepsis

0

Amniotic fluid embolism

0

Saline induced abortion

0

Hemorrhage
0

II. MANIFESTATIONS
• Bleeding at sites of modest trauma
• Bleeding from venipuncture site, nicks from shaved area of perineum or abdomen,
trauma from insertion of a catheter
• Bleeding from the gums or nose
• Petechiae and purpuric rash

III. DIAGNOSIS
• Excessive bleeding
Bioassay • Purpura and petechiae at pressure sites
• Surgical procedure with intractable bleeding
• Fibrinogen (300-600 mg/dL)
• Elevated fibrin and degradation product levels
Laboratory
• Decreased platelet count (thrombocytopenia)
tests
• Prolonged prothrombin time (PT) & partial thromboplastin time (PTT)
• Elevated D-dimer levels

IV.MANAGEMENT
• Cornerstone of the therapy: eliminate or treat the triggering process (i.e., prompt
identification and removal of inciting source of the coagulopathy)
• Replacement of pro coagulants for planned or anticipated extensive surgeries (e.g.,
transfusion of blood components)
• Vigorous restoration and maintenance of circulation to treat hypovolemia

207
 SECTION FOUR
POSTPARTUM HEMORRHAGE
OVERVIEW OF POSTPARTUM HEMORRHAGE (PPH)
• An obstetric emergency
• Normally, hemostasis occurs upon placental separation because uterine bleeding is
controlled by a combination of two mechanisms:
° Contraction of the myometrium, which compresses the uterine sinuses and vessels
0Local decidual hemostatic factors which cause clotting

I. DEFINITIONOF TERMS
• The following are suggested definitions of postpartum hemorrhage but there is a lack of
agreement on what constitutes excessive blood loss:

• Blood loss 2'500 mL for vaginal delivery and > 1,000 mL for CS
POGSCPG • Blood loss ;;,500 mL in the first 24 hours following delivery
0
10% decrease in hemoglobin or hematocrit level
0
Need for transfusion
• 2'1000 mL blood loss regardless ofroute of delivery accompanied
Williams, 25th ed.
by signs and symptoms ofhypovolemia
Source:POGSCPGon ThirdTrimesterBleeding
and PostpartumHemorrhage.
November 2012
Williams'
Obstetrics.25thed. 2018

A. Definition of Obstetric Hemorrhage Combining Clinical and Objective Data

I VOLUME
BLOOD HEART
I SYSTOLIC BP I SIGNS AND
BLOOD LOSS
I RATE SYMPTOMS
500-1000 mL 10-15% <100 bpm Normal • None

1000 -1500 mL 15-25% 100-120 bpm Slight decrease • Vasoconstriction

• Weakness

1500-ZOOOmL 25-35% 80-100 mmHg • Restlessness,

120-140 bpm
pallor, oliguria

2000-3000 mL 35-45% >140 bpm 60-B0mmHg • Anuria, altered

consciousness
Source:Bonnaret al. 2000
B Cl 'fi t· fH h :
CLASS I BLOOD LOSS I SIGNS & SYMPTOMS*
• Minimal tachycardia
I 500 mL to 1 liter
• No change in BP,pulse pressure, RR or capillary refill
• Mild tachycardia and tachypnea
II ~2 to 3 liters
• Decrease in pulse pressure
• Reduction in systolic BP
III ~3 to 4 liters
• Significant tachycardia and tachypnea
• Marked tachycardia; significant depression of systolic BP
IV >4 liters • Narrow pulse pressure
• Skin is cold and pale
'Postpartumhemorrhageis "treacherous"
- pulserateand bloodpressuredo notundergomorethanmoderate
alterationsuntilmassiveamountsofbloodhavebeenlost
Source:Committee on Trauma,AmencanCollegeofSurgeons;2008

208
C Class1"fication base d on 0 nset of Hemorrhal!e
Third Stage
• Postpartum hemorrhage before placental delivery
Hemorrhage
Early Postpartum
• Blood loss of> 500 mL during the first 24 hours after delivery
Hemorrhage
Late Postpartum
• If bleeding occurs after 24 hours to 12 weeks after delivery
Hemorrhage
ObstetGynecol;2017
Source:Committeeon PracticeBulletins-Obstetncs.

II. ETIOLOGYAND RISK FACTORS

• PPH occurs in response to an abnormality of one of 4 basic processes ("4 T's"):
0 Tone: uterine atony
Tissue: retained placental tissue or blood clots
0 Trauma: genital tract lacerations or hematomas
0 Thrombin: coa ulo ath

• Multiple gestation
Overdistended uterus • Polyhydramnios

■
• Macrosomia
Tone • Prolonged labor
(Abnormal Uterine muscle fatigue • Augmented labor
uterine • Prior postpartum hemorrhage
contractility)
Chorioamnionitis • Prolonged rupture of membranes (ROM)

Uterine distortion/abnormality • Fibroids (myoma), placenta previa

Uterine relaxing drugs • Beta-mimetics, MgS04, anesthetic drugs
• Prior uterine surgery
Tissue Accreta/increta/percreta • Placenta previa
(Retained • Multiparity
products of
conception) • Manual placenta removal
Retained placenta/membranes
• Succinturiate/accessory lobe
• Precipitous delivery
• Macrosomia
Laceration of the cervix, vagina or
• Shoulder dystocia
perineum
• Operative delivery
• Episiotomy ( e.g. mediolateral)
Trauma
(Genital tract • Deep engagement
Extension of incision/laceration
trauma) • Malposition
at CS
• Malpresentation
Uterine rupture • Prior uterine surgery
• Fundal placenta
Uterine inversion • Grand multiparity
• Excessive traction on umbilical cord
Preexisting clotting abnormalities
(e.g. hemophilia, von Willebrands • History of coagulopathy or liver disease
disease, hypofibrinogenemia)
Thrombin • Sepsis
(Abnormalities DIC • Excessiveblood loss
of coagulation) • Long-standingintrauterine demise
• Severe preeclampsia
HELLP
• Intrauterine demise
Anticoagulation • Hemorrhage
Sources: POGSCPG on ThirdTrimesterBleedingand PostpartumHemorrhage.2012,Bonnaret al. 2000
209
III. MANIFESTATIONS OF POSTPARTUM HEMORRHAGE
A. Signs and Symptoms of Hemorrhagic Shock
SYSTEM I EARLY SHOCK I LATE SHOCK
CNS • Altered mental status • Obtunded
• Tachycardia, orthostatic • Cardiac failure, arrhythmias,
Cardiac
hypotension hypotension
Renal • Oliguria • Anuria
Respiratory • Tachypnea • Tachypnea, respiratory failure
Hepatic • No change • Liver failure
GIT • No change • Mucosal bleeding
Hematologic • Anemia • Coagulopathy
Metabolic • None • Acidosis, hypocalcemia, hypomagnesemia

B. Classification of Hemorrhagic Shock

SYSTEM
I
BLOOD
LOSS
I
HEART
RATE I BP I c~LL YI
uo
[mL/hr)
I MENTAL
STATUS

Normal or
Compensated <l,000 mL <100 bpm Normal Normal >30
agitated
1,000 to Orthostatic Maybe
Mild >100 bpm 20-30 Agitated
1,500 mL change delayed
1,500 to Marked Usually
Moderate >120 bpm 5-20 Confused
2,000 mL fall delayed
Profound Always Lethargic,
Severe >2,000 mL >140 bpm Anuria
fall delayed obtunded
Source:MartelMJ.J ObstetGynaecolCan;2018

IV.GENERALMANAGEMENTOF POSTPARTUMHEMORRHAGE(PPH)
• Simultaneous, coordinated, multi-disciplinary management (OB-GYN,anesthesiologist,
hematologists, radiologists, nurses, laboratory and blood bank technicians) to concur
timely management in the presence of obstetric hemorrhage
• Preoperative preparedness is important especially for patients identified as high risk
• Details in the management (depending on etiology) are discussed in the succeeding section

A. Initial Management

I
INITIAL
REMARKS
APPROACH
• Constant awareness of the hemodynamic status as well as evaluation
Assessment
to determine the cause of bleeding.
Breathing • Administration of oxygen
• Obtaining intravenous (IV) access and adequate circulating blood volume
through infusion of crystalloid and blood products
Circulation
• Second large-bore IV catheter is needed
• Notify the blood bank

210
 B. Review of the Management of the Third Stage of Labor
APPROACH I COMPONENTS
• Recommended by guidelines
• Consists of (discussed in detail below):
Active 0 Routine administration of a prophylactic uterotonic just before
management of
labor or immediately after the birth of the baby
0 Delayed cord clamping
° Controlled cord traction to deliver the placenta

• Allows spontaneous delivery of the placenta by awaiting the signs

Expectant or of placental separation, or with the aid of gravity, maternal pushing
conservative
or nipple stimulation
(physiologic)
management of
• Prophylactic uterotonic is not administered
labor • Umbilical cord is neither clamped nor cut until the placenta has
been delivered

1. Uterotonics
I

■
UTEROTONIC REMARKS
• Preferred uterotonic in the active management of the third stage of
labor because of fewer side effects, but similar efficacy with others
• Can also be used in CSdeliveries
Oxytocin
• Preferred route for oxytocin is intravenous
• There is still insufficient evidence to issue a recommendation as to the
timing of giving oxytocin (before or after placental delivery)
• May be used in cases where PPH is refractory to oxytocin
• Should only be given in the presence of trained personnel
Carboprost
• Should not be given among patients with increased intraocular
(IM)
pressure, hypertension/hypotension, cardiovascular /pulmonary/
renal disease, anemia, epilepsy and jaundice
• Ergometrine
Other agents • Syntometrine
• Carbetocin

2. Delayed Cord Clamping

• Delayed cord clamping (> 1 minute up to 3 minutes) should be practiced over early cord
clamping (30-60 seconds of birth):
• For infant benefit with regards iron status
• May have some prevention of PPH
• In cases of neonatal asphyxia, cord should be immediately clamped for early resuscitation

3. Controlled Cord Traction to deliver the Placenta

• Can be used to shorten the third stage of labor and to further minimize blood loss when
skilled birth attendants are available and oxytocin is the primary uterotonic
• In CS,the placenta should be primarily removed through cord traction

V. IMPORTANTCAUSESOF POSTPARTUMHEMORHAGE
• Uterine atony
• Retained placenta
• Uterine rupture
• Uterine inversion
• Genital tract trauma

211
UTERINE ATONY
• Most frequent cause of obstetrical hemorrhage
• Women with risk factors for uterine atony should be delivered in a hospital with adequate
facilities to manage PPH

I. ETJOPATHOGENESIS
A. Pathogenesis
° Caused by the failure of the uterus to contract sufficiently after delivery and to arrest
bleeding from sinuses at the placental implantation site

B. Risk Factors
0 Primiparity or multiparity
0 Overdistended uterus (e.g., women with large fetus, multiple fetus, or hydramnios)
0 Labor abnormalities

0Labor induction or augmentation

0Prolonged third stage
0 Prior postpartum hemorrhage
0 Use of excessive concentrations of halogenated anesthetics that will relax the uterus

II. MANIFESTATIONS & DIAGNOSIS

• Uterus is soft and not well contracted (hypotonic)
• Profuse vaginal bleeding

III. MANAGEMENT
A. Overview
• Active management of the 3rd stage of labor with use of uterotonics
(most important component)
• Drugs:
0 Oxytocin: given IM or via IV infusion after placental delivery
Pharma co logic
0 Methylergonovine (Methergine): second-line treatment;
contraindicated in hypertensive patients
0 Prostaglandin analogues: carboprost, misoprostol
0 Oxytocin analog: carbetocin
• Vigorous fundal massage
• Bimanual uterine compression, balloon tamponade
• If ineffective: B-Lynch procedure, internal iliac artery ligation,
Non-
hysterectomy
pharmacologic
• Uterine artery embolization
• Manual placental removal: indicated when heavy bleeding persists
after delivery & while placenta remains partially or totally attached
Source:CPG on ObstetricHemorrhage.POGS;2014

B. Clinical Practice Guidelines

• Conservative, non-surgical measures in the management of uterine a tony may be
performed if bleeding persists after standard treatments (i.e., bimanual uterine
compression, balloon tamponade)
• Brace compression suture procedures may be performed for uterine a tony if bleeding
persists after standard and nonsurgical measures (i.e., B-Lynch procedure)
• If uterine compression strategies are ineffective, ligating blood vessels supplying the
uterus may mitigate bleeding long enough until uterine contraction and clotting catches
up (either by a uterine artery or internal iliac artery ligation)
• If all attempts fail, a partial or a total hysterectomy is performed
Source:CPGon ObstetricHemorrhage.POGS;2014

212
C. Some Maneuvers/Procedures

• Done by placing a hand in the

vagina pushing against the
body of the uterus anteriorly
Bimanual in a cephalad direction with
uterine
compression the other hand abdominally
compressing it in a caudal
4~~
direction while keeping the
uterus in anterversion

• Increases the intracavitary

uterine pressure by inflating
a medical grade balloon in the
uterus with saline solution ■
until the myometrial walls are _-•
Uterine distended enough to compress ; ..
balloon
the uterine sinuses to stop the
tamponade
(Bakri) bleeding
• Pressure is gradually lessened
by releasing fluid from balloon
in increments until the uterus
is contracted enough that no
further bleeding is observed

Uterine • Application of suturing on the

compression atonic uterus to mechanically
sutures compress uterine sinuses to
(B•Lynch
procedure) stop the bleeding

213
RETAINED PLACENTA OR PLACENTAL FRAGMENTS
I. RETAINEDPLACENTA
• Retention of the placenta in utero for >30 minutes
• More common cause of late postpartum bleeding (after the first 24 hours)
• The bleeding may be visible or may manifest only by the increasing size of the uterus
In the absence of any evidence of placental detachment, consider the diagnosis of
complete placenta accreta or a variant.

Management of Retained Placenta

• If placenta is not expelled spontaneously, may give 10 IU ofoxytocin in combination with
controlled cord traction*
• lntraumbilical vein injection of oxytocin with saline may be offered for the management of
retained placenta
• If the placenta is still not delivered, manual extraction of the placenta should be offered as the
definitive treatment. Antibiotics may be given offered after manual removal of the placenta
• Rule out placenta accreta
'Ergometrineis not recommendedbecause it may cause tetanic uterinecontractions,whichmay delay expulsionof
the placenta. ProstaglandinE2 (PGE2)(dinoprostoneor sulprostone)is also not recommended.
Source: CPG on ObstetricHemorrhage.POGS;2014, 2019

II. RETAINEDPLACENTAL
FRAGMENTS
• May interfere with the complete uterine involution preventing adequate compression of
the uterine sinuses and vessels at the exposed placental implantation site
• Manifests as late postpartum hemorrhage, presenting as prolonged postpartum bleeding
• May be avoided by awaiting signs of placental separation before delivering placenta and
inspecting the placenta for completeness upon delivery

Mana.aement of Retained Placental Fraaments

• Suspicion of retained placental segments associated with an open cervix and subinvoluted
uterus may be confirmed by ultrasound
• Management may be done by doing manual removal of the secundines or by curettage under
anesthesia
• Uterotonics and antibiotics may be given as necessary
Source: CPG on ObstetricHemorrhage2nd Edition.POGS, Inc;2019

214
UTERINE RUPTURE
I. ETIOPATHOGENESIS
• Rare & catastrophic complication with a high incidence of fetal and maternal morbidity
• Usually involves a thinned out lower uterine segment or a weakened uterine scar

A. Etiology
ETIOLOGY I REMARKS
• Surgery involving the myometrium: CS,previously repaired
uterine rupture, myomectomy, cornual resection of the interstitial
Preexisting
fallopian tube
uterine injury or
anomaly • Coincidental uterine trauma: abortion with instrumentation, trauma
• Congenital: connective tissue disorder, pregnancy in undeveloped
uterine horn
• Before delivery: labor stimulation, uterine overdistension, external
Uterine injury version

I
or abnormality
• During delivery: internal version of 2nd twin, difficult forceps
incurred
delivery, difficult manual removal of placenta
in current
pregnancy • Acquired: placenta accrete, adenomyosis, gestational trophoblastic
neoplasia ; :

B. Classification of Uterine Rupture

CLASSIFICATION I REMARKS
Primary • Occurring in a previously intact or unscarred uterus
• Associated with a preexisting incision, injury, or anomaly of the
Secondary
myometrium

C. Patients who are High Risk of Pregnancy-Related Uterine Rupture

0 Most direct prevention strategy to minimize risk of uterine rupture is to minimize the
number of patients who are at high risk
0 If any gravid falls into any category below, her risk for rupture is >l in 200:
• Previous CS delivery:
• with an interdelivery interval of <2 years
• without a previous history of a successful vaginal birth
• with either labor induction or augmentation
• in a woman carrying a macrosomic fetus >4000 grams
• classical CS delivery
• via low vertical CS delivery
• via low transverse CS delivery with a congenitally abnormal uterus
• via low transverse CS delivery with a single-layer hysterotomy closure
• Several previous CS deliveries
• Previous uterine myomectomy accomplished by means oflaparoscopy or laparotomy

Source:CPGon ThirdTrimesterBleedingandPostpartum
Hemorrhage.
POGS,Inc;2009

II. MANIFESTATIONS
• Initial manifestations are nonspecific, which makes the diagnosis difficult and sometimes
delays definitive therapy:
Fetal distress (evidenced by pattern of abnormalities in FHR)
0 Recession of the presenting fetal part into the maternal pelvis
Diminished baseline uterine pressure or loss of uterine contractility
Abnormal labor pattern or failure oflabor to progress, abdominal pain
, Hemorrhage and shock
• Fetal morbidity occurs as a result of catastrophic hemorrhage, fetal anoxia, or both.

215
III. UTERINERUPTUREVERSUSDEHISCENCE
• Uterine rupture: separation of old uterine scar throughout most of its length with rupture
of fetal membranes (uterine cavity and peritoneal cavity communicate)
• Uterine dehiscence: occult and incomplete disruption that does not lead to any serious
maternal or neonatal consequences

UTERINE
DEHISCENCE

• All layers disrupted

(extending into
• Fetal membranes
peritoneum)
are not ruptured
leading to • Not all layers
Description and the fetus is
communication disrupted
not extruded into
between the uterine
peritoneal cavity
and the peritoneal
cavity
Visceral
• Ruptured • Intact • Intact
peritoneum
Fetal parts • Intra-abdominal • Uterine • Uterine
Bleeding • Minimal to massive • Absent or minimal
Uterine scar
• Nearly whole length • Segmental
separation
Bag of water{BOW) • Ruptured • Intact
Source:CPG on ObstetricHemorrhage2nd Edition.POGS, Inc;2014,2019

IV.MANAGEMENT
• Definitive therapy for the fetus is immediate abdominal delivery.
• Conservative surgical management involves revision of the edges of the prior incision
following primary closure and should be reserved for women who have the following
findings:
0 Type of uterine rupture: low transverse uterine rupture
0 Extent of rupture: no extension of the tear to the broad ligament, cervix, or paracolpos.
0 Degree of hemorrhage: easily controllable uterine hemorrhage
0 General condition of the mother: hemodynamically stable
0 Desire for future childbearing
0 No clinical or laboratory evidence of an evolving coagulopathy
• Hysterectomy is the treatment of choice when intractable uterine bleeding occurs or when
the uterine rupture sites are multiple, longitudinal, or low lying.
Source:CPG on ObstetricHemorrhage2nd Edition.POGS, Inc:2014,2019

216
UTERINE INVERSION
• Inside-out displacement of the fund us of the uterus during the third stage of labor
• Prevents myometrium from contracting and retracting, and it is associated with life-
threatening blood losses as well as profound hypotension from vagal activation

I. ETIOPATHOGENESIS
• Rare condition, occurring in 0.05% of deliveries
• Almost always due to vigorous traction of the umbilical cord prior to detachment of a
fundally implanted placenta

A. Etiology:
, Overly aggressive management of the third stage of labor
, Excessive umbilical cord traction while the uterus is relaxed
, Extrinsic factors: use of magnesium sulfate or oxytocin (some studies)
, Intrinsic factors:
• Primiparity
• Uterine hypotonia secondary to twin pregnancy and use of P-mimetics
• Placenta accrete (involving the uterine fundus)
• Fundal myoma
• Short umbilical cord

■
• Rapid emptying of the uterus after prolonged distention
• Congenital weakness or anomalies of the uterus

B. Risk Factors
'Fundally implanted placenta
, Uterine atony
'Cord traction applied before signs of placental detachment, which are:
• A sudden gush of blood
• Lengthening of the visible portion of the umbilical cord
• Uterus becomes globular and firm
• Uterus rises to the abdomen
, Abnormally adherent placentation

II. MANIFESTATIONS
• Clinical signs and symptoms: hemorrhage, shock and severe pelvic pain
• Bimanual exam will confirm the diagnosis and reveal the degree of inversion.
Uterus not palpable abdominally in complete uterine inversion
, Internal examination shows a palpable mass

A. Classification based on Onset after Deliverv:

• Immediately or within 24 hours after delivery
Acute inversion
• Most common type
Subacute inversion • After 24 hours and within 4 weeks after delivery
Chronic inversion • >4 weeks after delivery
2ndEdition.POGS,Inc;,2019
Source:CPGon ObstetricHemorrhage

B. Classification based on Anatomical Severity:

1st stage • Uterine base is in the uterine cavity

(Incomplete/ and do not cross the cervix
Partial)

2nd stage • Uterine base crossed the cervix and

(Complete) passed through vagina

• Visualization of the uterine base at

3rd stage
the vulva

4th stage • Vaginal walls participate with the

(Prolapsed) inversion.
FG,et al. WilliamsObstetrics25thEd;2018
Source:Cunningham
217
III. DIAGNOSIS
• Imaging can help when the diagnosis is uncertain after examination, and the patient is
sufficiently stable clinically to undergo such evaluation. (e.g. ultrasound, MRI)
• The fundus attached to the placenta on delivery looks like a round mass protruding from
the cervix or vagina accompanied by profuse bleeding

IV.MANAGEMENT
• Application of active management of the third stage of labor including controlled cord
traction decreases incidence of acute uterine inversion following vaginal delivery

AO verv1ew o fM anagement
• Tocolysis may be initiated, if necessary to relax the uterus
• If uterus has not contracted & has retracted completely and placenta
has separated, uterus is replaced by pushing up on the inverted fund us
with the palm and fingers* in the direction of the long axis of the vagina
Manual • If placenta is still attached, attempts are made to reposition with the
replacement placenta in situ. After uterus is replaced, placenta is manually removed
ofuterus and delivered
• If uterine repositioning fails with placenta attached, it is peeled off and
steady pressure with fist, palm, or fingers* is applied to the inverted
fundus in an attempt to push it up into and through the dilated cervix
• Once uterus is repositioned, tocolysis is stopped and oxytocin is infused
• Done when manual replacement fails (possible cause: tight myometrial
Surgery constriction ring)
• Exploratory laparotomy, Huntington procedure, Haultain incision
'Cautionis observedwheneverusingthe fingersin repositioningthe uterusto preventperforation

B. Management of Uterine Inversion

• Prompt replacement of uterus (see methods below) with or without general anesthesia
and/or tocolytics (e.g. terbutaline, MgSO4, nitroglycerin for uterine relaxation)
• If placenta is still attached, it should be left in place until after reduction (i.e., Johnson
maneuver)
• If the above method is unsuccessful after another attempt, consider Iaparotomy or
transvaginal cervical incision & repair (see surgical replacement or laparotomy methods
below)
• Uterotonic drugs should only be given immediately after repositioning of the uterus.
• Hysterectomy is the last resort for any of the following conditions:
0 Repositioning and medical treatment have failed
0 Gangrenous uterus
0 Intractable hemorrhage due to atony after successful repoisitioning
• Antibiotic prophylaxis is advisable (decision is left to the discretion of the provider]
Source:CPGon ObstetricHemorrhage2nd Edition.POGS,Inc;2014,2019

C.WHO Recommendations Regarding Antibiotic Prophylaxis

Single dose of prophylactic
antibiotics after repositioning
If with signs of infection, give
combination antibiotics (until
afebrile for 48 hours)
• Ampicillin 2 g/lV or Cefazolin 1 g/IV, PLUS
• Metronidazole 500 mg/IV
• Ampicillin 2 g/lV every 6 hours
• Gentamicin 5 mg/kg body weight IV every 24 hours
• Metronidazole 500 mg/IV every 8 hours

218
D. Replacement of the Uterus
METHOD I ABORTION
Initial Replacement
• Patient is placed in lithotomy position and two bottles of 1 liter
warm (40°C) irrigation fluid (0.9% NSS) are attached to a cystoscopy
irrigation set
Hydrostatic • Nozzles of the rubber tubes should be directed to the posterior fornix
reduction of the vagina
(O'Sullivan
hydrostatic • Run the warmed fluid by gravity or pressure and prevent the water
maneuver) from leaking out of the vagina (up to 4 liters may be required)
• As the vaginal wall distend, the fundus and the uterus will begin to rise
• Reduction can be achieved in about 5-10 minutes
• After complete replacement, start oxytocin drip & give ergometrine IV
• Grasp the inverted uterus with the placenta with one hand
• The fundus is allowed to rest on the palmar surface of the operator's
hand with fingertips exerting equal pressure around the collar of the
uterus within the cervical opening

■
• The fundus is then replaced with upward pressure
Johnson
• After repositioning the uterus, the placenta is manually removed
maneuver
followed by uterine exploration
• Operator's hand is kept inside the uterus, slowly removed as it begins
to contract around the hand
• A tight uterovaginal pack may be inserted before the hand is removed
from the uterine cavity (pack can be removed after 24 hours)
Surgical Replacement
• Grasping the round ligaments to locate the depression of the uterine
fundus formed by the inversion
Huntington
• Clamps are placed on the inverted fund us below and within the
procedure
cervical ring, and gentle upward traction is applied
• Repeated clamping & traction continues until inversion is corrected
• Incision is made on the uterine wall at the posterior rim of the cervical
ring
• Length of the incision should be sufficient to permit passage of the
Hultain uterine fundus
procedure • Fundus is restored by combined traction on the uterine wall from
above by the surgeon and pressure from the vagina by an assistant
• When the uterus is completely restored, the incision is closed with
interrupted sutures
Source:CPGon ObstetricHemorrhage2nd Edition.POGS,Inc;2014,2019

219
GENITAL TRACT TRAUMA
• Genital tract traumas are the second most common causes of PPH (20%)
• Includes lacerations to the perineum/vagina/cervix, large episiotomy (including
extensions)
• Types of genital tract trauma:
Genital tract lacerations (1st, 2nd, 3rd, and 4th degree)
0 Genital tract hematoma

I. GENITALTRACTLACERATION
• Occurs at the vaginal vault as the fetal head passes through
• It can involve the perineum, vagina and the cervix
• Genital tract laceration should be suspected if bleeding will persist despite a well-
contracted uterus

A. Types of Lacerations
1. Perinea! Lacerations
• Trauma may occur spontaneously or arise from episiotomy during vaginal delivery
• May reach to involve the anal sphincter (causing incontinence & rectovaginal fistula if
untreated)
CLASSIFICATION I REMARKS
Classificatio'l, by Location_ Pi'

Anterior perinea I • Injury involving the labia, anterior vagina, urethra or clitoris
trauma
Posterior perinea! • Injury to the posterior vaginal wall, perinea! muscles or anal
trauma sphincters and may extend through the rectum
- --
Classificatiortlbase_don Depth or Degr,ee
• Fourchette, perinea! skin, and vaginal mucous membrane
1st degree
• Does not reach the underlying fascia and muscle
• Aside from skin and mucous membrane, the fascia and
2nd degree
muscles of the perinea! body are involved
• Lacerations extend through skin, mucous membrane, perinea!
body and anal sphincter
• Royal College of Obstetricians & Gynecologists (RCOG)
3rd degree subclassification:
0 3a: <50% of external anal sphincter thickness torn
0 3b: >SO% of external anal sphincter thickness torn
0 3c: internal anal sphincter torn
• Extension of laceration through the rectal mucosa to expose
4th degree
lumen of the rectum

2. Vaginal Lacerations
• Associated with forcep/vacuum deliveries or in precipitous deliveries
• May extend to the underlying tissues and cause significant hemorrhage
• Considered if there is vaginal bleeding while the uterus is firmly contracted

3. Cervical Lacerations
• lntrapartum cervical lacerations are more common and most are asymptomatic
• Suspected in cases of profuse bleeding if uterus is well contracted
• Cervix should be routinely inspected after the 3rd stage of labor in all difficult
deliveries, even if there is no bleeding
• Any cervical tear, which is actively bleeding and/or >2 cm in length should be sutured
• May be incurred during forceps deliveries when performed through an incompletely
dilated cervix with the blades applied over the cervix

220
B. Prevention of Genital Tract Lacerations
0 Optimize episiotomy to reduce occurrence of severe perinea! trauma
0 Minimizing operative vaginal delivery can decrease incidence of trauma (vacuum
extraction is less associated with severe perinea! trauma compared with forceps)
0 Antenatal perinea! massage reduces perinea! trauma

C. Management of Genital Tract Lacerations

0Leaving perinea! skin unsutured to heal by secondary intention reduces dyspareunia
and pain up to 3 months.
Any cervical tear, which is actively bleeding and/or >2 cm in length should be sutured
0

to prevent cervical incompetence

0In repairing genital tract lacerations, an anchoring suture is placed 1 cm above the
apex of the vaginal tear and/or episiotomy incision, and just above the angle of the
cervical lacerations for adequate hemostasis

LOCATION OF RECOMMENDED SUTURE

LACERATION I MATERIAL* I SUTURING TECHNIQUE**

• Continuous subcuticular suture

for repair of perinea! skin

■
• Polyglycolic acid and
Perineum • Loose, continuous, non-locking
Polyglactin 910
to appose the vaginal tissue,
perinea! muscle and skin

Actively bleeding • 2-0 polyglactin or 3-0 PDS

• Interrupted or running
cervical tear or absorbable sutures with
sutures
tear>2 cm tapered needle
External Anal • Monofilament (polydiaxanone) • Overlapping or end-to-end
sphincter or braided suture (polyglactin) approximation
Internal Anal • 2-0 polyglactin or 3-0 PDS
• Interrupted sutures
sphincter absorbable sutures
·Absorbablesyntheticmaterial(polyglycolic acid and polyglactin910) is preferred(less perinea!pain,analgesic
use, dehiscenceand resuturing)
.. Obliterationof dead spaces and preventionof overtightenedsutures shouldbe ensured when repairinggenital
tract lacerations.
Source:CPG on ObstetricHemorrhage2nd Edition.POGS, Inc;2014, 2019

D. Post-Operative Care and Follow-Up

0 Vaginal & rectal examination post-operatively should be done to check for bleeding,
hematoma, and ensure that suture material has not been accidentally inserted through
the rectal mucosa
0 To check effective repair of the anal sphincters, ask the patient to contract the anus
around the examining rectal finger
0 Broad-spectrum antibiotics is recommended following Obstetric Anal Sphincter
Injuries (OASIS) repair to reduce postoperative infections and wound dehiscence.
0 Post-operative laxatives are recommended to reduce the incidence of post-operative
wound dehiscence
0 All women who have had OASIS repair should be reassessed 6-12 weeks postpartum
for incontinence
0 Women may resume sexual intercourse at 3 to 6 months after repair of laceration
Source:CPG on ObstetricHemorrhage2nd Edition.POGS, Inc;2019

221
II. GENITALTRACT HEMATOMA
• Pregnant uterus, vagina and vulva have rich vascular supplies that are at risk of trauma
during the birth process, and trauma may result in formation of a hematoma
• Hema to mas are rarely a potentially life-threatening complication of childbirth.
• Good surgical technique, with attention to hemostasis in the repair of lacerations, should
limit the occurrence of puerperal hematoma

A. Classification of Genital Tract Hematomas

CLASSIFICATION I REMARKS
• May involve the vestibular bulb or branches of the pudenda! artery
(inferior rectal, perinea!, and clitoral arteries)
• Limitedto the vulvar tissues superficialto the anterior urogenital diaphragm
Vulvar hematoma
• Bleeding is then directed toward the skin and the loose subcutaneous
tissues exert little resistance to hematoma formation
• Manifests as pain and swelling in the perineum
• May involve the descending branch of the uterine artery
• Collection of blood in the ischiorectal fossa
• Most vaginal or paravaginal hematomas often blocks the vaginal canal
Vaginal or
• Commonly associated with operative vaginal deliveries
Paravaginal
• Manifestations: rectal pain, vague lower abdominal pain, degree of
hematoma
shock that is not proportional to perceived blood loss
• May not be obvious externally but can be palpated through vaginal
examination
• Continued bleeding may dissect retroperitoneally to form a mass
Retroperitoneal
palpable above the inguinal ligament
hematoma
• Occasionally fatal

B. Manifestations
0 Excessive perinea] pain is the hallmark symptom
° Change in vital signs disproportionate to the amount of blood loss should prompt a
gentle pelvic examination
0 Non-specific signs and symptoms may also present (e.g. pressure symptoms, swelling,
urinary retention, unexplained pyrexia)

C. Diagnosis
0 Other than the usual tests for bleeding and imaging may be helpful to confirm the
diagnosis when there is a suspicion for hematoma but the patient remains stable
0 Ultrasound, CT scan, or MRI:
• Mainly useful for diagnosing hematomas above the pelvic diaphragm
• Useful to assess any extension into the pelvis, particularly as bimanual examination
may not detect them until they become quite large and palpable

D. Management of Genital Hematomas

Early recognition followed by timely intervention
0

Identify the source of bleeding, then ligate and suture

0

Prevent further blood loss by any of the following:

0

• Vaginal packing
• Balloon tamponade or blood pressure cuff tamponade
SCENARIO
I MANAGEMENT
Small, non-expanding • Can be managed conservatively (e.g., ice pack, pressure dressing
hematoma (<3 cm) and analgesia)
Large hematomas • Best managed with surgical evacuation, primary closure and
(;;,3cm) compression for 12-24 hours
• Additional surgical intervention is indicated (e.g.,ligation of the
Hematomas with
internal iliac artery, hysterectomy, selective arterial embolization)
intra-abdominal pelvic
extension • Embolization of the bleeding vessel may be a therapeutic if
bleeding is not life threatening
Source:CPGon ObstetricHemorrhage
2ndEdition.POGS,Inc;2014,2019
222
REFERENCES
l.Bailit JL, Grobman WA, Rice MM, et al: Morbidly adherent placenta treatments and outcomes. Obstet Gynecol 125(3):683,
2015
2.Belfort MA.Overview of postpartum hemorrhage. https://www.uptodate.com. Accessed June 14, 2021
3.Bonnar /. Baillieres Best Pract Res Clin Obstet Gynaecol 2000; 14:1
4.Callahan, Tamara L. (2013). Blueprints obstetrics & gynecology. Baltimore, MD :Lippincott Williams & Wilkins
S.Capitulo RB. Uterine Rupture. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice Guidelines
on Obstetric Hemorrhage. November 2019.
6.Committee on Trauma, American College of Surgeons. Advanced trauma life support for doctors-student course manual. 8th
ed. American College of Surgeons, Chicago2008
7.Cummings K, Doherty DA, Magann EF, et al: Timing of manual placenta removal to prevent postpartum hemorrhage: is it
time to act? J Matern Fetal Neonatal Med 29(24):3930, 2016
8.Cunningham, F.G.. Leveno, K. J.. Bloom, S. L.. Spong, C.Y.,Dashe, J. S., Hoffman, B. L.,Sheffield, J. S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
9.Cunningham, F.G., Leveno, K. /., Bloom, S. L., Spong, C.Y.,Dashe, J. S., Hoffman, B. L.,Sheffield, J. S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
10. Dee MT.Retained Placenta. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice Guidelines
on Obstetric Hemorrhage. November 2019.
11. Driessen M, Bouvier-Colle MH, Dupont C, et al: Postpartum hemorrhage resulting from uterine a tony after vaginal delivery.
Factors associated with severity. Obstet Gynecol 117(1):21, 2011
12. Festin, M. (2008). Manual of Obstetric and Gynecologic Emergencies. Manila: Publications Program. ■
13. Fro Iova Al, Stout MJ,Tuuli MG,et al: Duration of the third stage oflabor and risk of postpartum hemorrhage. Obstet Gynecol · -
127(5):951, 2016 ....
14. Hernandez-Quevedo MC. Uterine Inversion. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical •
Practice Guidelines on Obstetric Hemorrhage. November 2019.
15. Martel MJ.No. 115-Hemorrhagic Shock. J Obstet Gynaecol Can. 2018;40(12):e874-e882. doi:10.1016/j.jogc.2018.10.004
16. Norwitz ER, Park JS. Overview of the etiology and evaluation of vaginal bleeding in pregnant women. https://www.
uptodate.com. Accessed June 14, 2021
17. Oxorn H. Human labor and birth (5th ed). Norwalk, CT Appleton & Lange; 1986
18. Plotti I~ Di Giovanni A, Oliva C, Battaglia F, Plotti G (November 2008). "Bilateral ovarian pregnancy after intrauterine
insemination and controlled ovarian stimulation". Fertil. Steril. 90(5): 2015.e3-5
19. POGSCPG on Obstetric Hemorrhage. 2nd Edition. November 2019
20. POGSCPG on Third Trimester Bleeding and Postpartum Hemorrhage. 2nd Edition. November 2012
21. Practice Bulletin No. 183: Postpartum Hemorrhage.Committee on Practice Bulletins•Obstetrics. Obstet Gynecol.
2017;130(4):el68.
22. Quevedo, M.C. (2014). Clinical Practice Guidelines on Obstetric Hemorrhage. Quezon City: Philippine Obstetrical &
Gynecological Society (Foundation), Inc.
23. Reyes LO. Genital Tract Trauma. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice
Guidelines on Obstetric Hemorrhage. November 2019.
24. Silver RM: Abnormal placentation: placenta previa, vasa previa, and placenta accreta. Obstet Gynecol 126(3):654, 2015a
25. Toral JA.Management of Ectopic Pregnancy: Expectant vs lnte,vention, Medical vs Surgical. Philippine Obstetrical and
Gynecological Society (Foundation), Inc. Clinical Practice Guidelines on Ectopic Pregnancy. November 2016.

223
 ISSUES
OBSTETRIC
GENERAL
COMPLICATIONS
AND
 SECTION ONE
PRETERM LABOR
OVERVIEW OF PRETERM LABOR
I. DEFINITION OF PRETERM LABOR
• Occurrence of regular uterine contractions associated with progressive cervical dilatation
and/or effacement before the completion of37 weeks AOG (term starts at 37 weeks)
CONCEPT I DEFINITION
• Refers to a fetus, pregnancy or neonate <37 weeks but is beyond the age
Preterm
of viability (20 weeks)
• Refers to a neonate that has the function expected of a newborn with age
of gestation less than 37 weeks
• It is best to use the AOG than the weight to determine if fetus is
Premature
premature or not ( a fetus may be large for gestational age, but is still
premature - also, a fetus may be small for gestational age and not be
premature)

II. ETIOPATHOGENESIS

■
A. Pathophysiology
0 Involves four (major) pathogenic processes that may overlap resulting in increased
contractility, membrane rupture and cervical ripening: '
• Activation of the hypothalamic-pituitary-adrenal (HPA) axis
• Infection and corresponding inflammatory response
• Decidual hemorrhage
• Pathologic uterine distention

B. Risk Factors of Preterm Labor

CATEGORY
I FACTORS
Non-Modifiable Antenatal Factors
• Ethnicity, age, marital status, short stature
Demographic • Unwanted pregnancy, shortened inter-pregnancy interval
• Male fetal gender
• History of prior preterm birth, indicated preterm birth, medically
Obstetrical
indicated preterm birth, prior D&C,previous CS
history
• Pregnancy resulting from assisted reproductive technology
...
i, Modifiable Factors ~

• Active or passive smoking

Behavioral • Illicit drug use, alcohol consumption
• Douching during pregnancy
• Maternal malnutrition (underweight or obese)
• Low pregnancy weight gain
Nutrition • Maternal anemia, vitamin D insufficiency
• Low consumption of fruits and vegetables
• Low levels of omega-3 fatty acids
• Socioeconomic status
Unknown • Prenatal maternal anxiety, maternal stress, depression
Modifiability
• History of intimate partner violence

Potentially • Long working hours, short sleep duration

Modifiable • Prolonged standing, lifting and carrying
Conditions • Infections (e.g., STl's, bacteriuria, periodontitis, vaginal infections)

227
III. CAUSESOF PRETERM LABOR
ETIOLOGY I REMARKS
• Early uterine distension acts to initiate expression of contraction-
Uterine
associated proteins (CAPs) in the myometrium
distension
• Examples: multifetal pregnancy, hydramnios
• Brought about by nutrient deficiency, obesity, maternal infection,
diabetes, psychological stress
Maternal-fetal
• Premature activation of the placental-adrenal endocrine axis increases
stress
placental-derived corticotropin-releasing hormone (CRH), leading to
early loss of uterine quiescence
Premature • Changes in the epithelial or stromal extracellular matrix
cervical
• Reduced mechanical competence of the cervix
changes
• Bacteria gain access to the uterine tissues through:
0 Transplacental transfer of maternal systemic infection
0 Seedings from the peritoneal cavity via the fallopian tubes
Infection 0 Accidental introduction during intrauterine procedures
0 Ascending infection with bacteria from vagina & cervix (most
common route)

MANIFESTATIONS AND DIAGNOSTIC EVALUATION

I. CLINICALDIAGNOSISOF PRETERMLABOR
Presence of uterine contractions (>4 every 20 minutes}, PLUS
• Cervical dilation >2 cm in nulliparous or >3cm in a multipara, OR
• Cervical effacement (>80%)

II. INITIAL EXAMINATION

EXAMINATION I RATIONALE
• Check for bleeding: placenta previa or abruptio placenta which can
trigger preterm labor
Speculum
• Evaluate fetal membrane status (i.e., intact versus ruptured)
examination
• Obtain cervicovaginal fluid for fetal fibronectin testing (although
sampling without a speculum is also acceptable)
Digital cervical
• Assess cervical dilatation and effacement (after placenta previa and
(internal)
rupture of membranes have been excluded by initial examination)
examination

III. OBSTETRICULTRASOUNDEXAMINATION
• Provides additional information:
0Determination of placental and fetal age
0Detection of fetal, placental, and maternal anatomic abnormalities
° Confirmation of fetal presentation
0Assessment of amniotic fluid volume
0Estimation of fetal weight

228
IV. TRANSVAGINALULTRASOUND
• Used to measure the cervical length and to check for the presence of cervical funneling
• Risk of preterm birth is higher if both a short cervical length and funneling are seen

A. Cervical Length
° Functional cervical length appears to be the best single cervical parameter to predict
spontaneous preterm birth
0A short cervix before 25 weeks AOG (length< 25 mm) indicates increased risk of
preterm birth

B. Cervical Funneling
0Defined as a protrusion of amniotic membranes into the internal cervical os by greater
than 5 mm from the shoulder of the original internal os
0Shape of the funnel indicates the degree of cervical dilation & effacement (see below)

T-SHAPE I Y-SHAPE I V-SHAPE I U-SHAPE

• With amniotic
• No funneling membrane
• More ominous finding
• Normal cervical protrusion into the
• Indicates more advanced cervical ripening
shape internal os with a
closed external os

■
'

DIAGNOSTIC I REMARKS
• Glycoprotein expressed during pregnancy, localized at the
choriodecidual junction, uterus, and placenta
• Checked in selected cases (see algorithm on the next page) to
Fetal
distinguish true preterm labor from false labor
fibronectin
• Subclinical infection/inflammation, abruption, or uterine contractions
releases fetal fibronectin into cervicovaginal secretions, which is the
basis for its use as a marker for predicting spontaneous preterm birth
• To diagnose asymptomatic bacteriuria, which is associated with an
Urine culture
increased risk of preterm labor /birth
• Rectovaginal group B streptococcal culture [antibiotic prophylaxis
Others depends on the results)
• Testing for sexually transmitted infections (e.g., chlamydia, gonorrhea)
Source: LockwoodCJ. Pretermlabor.Uptodate

229
CONCEPTS IN THE MANAGEMENT OF PRETERM LABOR
I. OVERVIEW OF MANAGEMENT
• Determination of fetal age and EFW (e.g., review history, ultrasonography)
• Corticosteroid administration
• Maternal transfer to a tertiary perinatal center
• Communication with a neonatologist
• lntrapartum monitoring
• Management of pain
• Preterm labor inhibition
• Method of delivery
• Resuscitation of the neonate

(+) Preterm uterine contractions,(+) BOW,

Reassuring maternal and fetal status,
No placenta previa or abruption

<34 weeks AOG ~34 weeks AOG

No tocolysis or
antenatal
corticosteroids
Admit for delivery if in
Cervix ~3 cm Cervix <3 cm labor OR
Send home if
contractionscease

TVS for cervical length

Cx <20 mm Cx 20-30 mm Cx ~30 mm

Fetal fibronectin

POSITIVE NEGATIVE

Preterm labor Preterm labor

LIKELY UNLIKELY

Tocolysis Observe for 4-6 hrs

Antibiotics for GBS Send home if NO
prophylaxis progressive ex
MgSO, (24-32 wks) dilatation and
for neuroprotection effacement
Corticosteroids Follow-up after 1-2
(23-34 weeks) if not weeks
imminent Follow-up if with
s/sx of PTL

Source:Lockwood,
et al. PretermLabor.UpToDate:
2019

230
II. GOALS OF PRETERM LABOR INHIBITION
• Achieve a 24- to 48- hour delay in the preterm delivery to administer
Immediate antenatal corticosteroids to hasten fetal lung maturity
goals • Transfer antepartum patient to a tertiary care facility for a higher level of
neonatal intensive care
• Maintain a sustained labor suppression to enable the fetus to mature in
Long-term utero and reach a gestation age as close to term as possible
goals • Reduce duration of hospital stay and number of hospital admissions for
recurrent preterm labor

lll. GUIDELINES FOR THREATENED & IMMINENT PREVIABLE DELIVERY

INTERVENTION I DESCRIPTION I <22

WEEKS
I 22
WEEKS
I 23
WEEKS
I ~23
WEEKS

• Includes stratification of
Neonatal
neonates who are likely to
assessmentfor
thrive outside utero with X C C ✓
resuscitation
intensive neonatal management
• Given to decrease neonatal
respiratory morbidity,
Corticosteroid

■
therapy
intracranial hemorrhage, X X C ✓
necrotizing enterocolitis, and
death .
Magnesium • Administered to reduce
sulfate occurrence of cerebral palsy X X C ✓

• To provide short-term
prolongation of pregnancy
enabling administration of
Tocolysis
antenatal steroids, magnesium X X C ✓
sulfate as well as transport to a
tertiary facility if needed
Continuous • Close antenatal surveillance to
EFM rule out fetal distress X X C ✓

Group B
Streptococci • GBS prophylactic antibiotics to
(GBS) improve neonatal outcomes X X C ✓
prophylaxis

• Planned Cesarean delivery

CS for fetal
indication
is done when extrauterine X X C ✓
resuscitation is indicated
Legend:
✓ Recommended
C Considergiving
X Notrecommended
Source:ACOG;2017
Rajuet al. ObstetGynecol;2014
CunninghamFG,et al. WilliamsObstetrics;2018

231
INDIVIDUAL COMPONENTS OF MANAGEMENT

I. TOCOLYTICAGENTS
• Drugs given to delay the delivery ofa fetus by inhibiting contractions ofmyometrial
smooth muscle contractions
• Given for at least 48 hours to permit completion of corticosteroid therapy
• Maintenance tocolysis is not associated with improved perinatal outcome and is therefore
not recommended routinely

TOCOLYTIC*
I EXAMPLES
I MECHANISM
I SIDE EFFECTS

• Nifedipine
• Tocolytic agent of
Calcium 30-40 mg/tab
first choice • Fetal: possible decrease in
channel (LD), then
• Inhibits the influx of uterine blood flow
blockers 30-160 mg/day
extracellular Ca2 •
in divided doses
;_c
• Monitor: urine output, deep
tendon reflexes, respiratory
• Not indicated as a rate.
• Magnesium primary tocolytic • Maternal: flushing, sensation
sulfate 4-6 g • Currently, more of warmth, nausea, emesis,
Neuro- slow IV over indicated for dizziness, nystagmus,
transmitter 20 minutes (LD), neuroprotection lethargy, pulmonary edema
blocker then infusion at • Reduces risk for • Antidote: Calcium
2 g/hourfor cerebral palsy gluconate 10 ml of10%
24-48 hours • Given between solution at bedside
24 - 32 weeks AOG • Fetal: nonreactive heart
rate, absent fetal breathing,
hypotonia, lethargy
• Terbutaline
• Maternal: hypotension,
5 mg PO Q4 or
tachycardia, arrhythmia,
0.25 mg SC for
pulmonary edema,
Beta- short-term use
• Reduces myometrial hyperglycemia,
adrenergic • Salbutamol
contractility hypokalemia
agonists 10 ug/min, up to
• Fetal: tachycardia,
45 ug/min
hyperinsulinemia with
• lsoxsuprine
hypoglycemia
• Ritodrine
• Maternal: flushing, nausea,
headache, dizziness,
palpitations, hypotension,
• Bind & inactivate
tachycardia
cyclooxygenase
• lndomethacin • Fetal: premature closure of
which regulates
50-100 mg (LD), ductus arteriosus with
Prostaglandin production of PGE2
then 25-50 mg consequent pulmonary
inhibitors to arachidonic acid
PO every 8 hours hypertension, persistent
• Category D if used
for 24-48 hours patent ductus arteriosus,
>48 hours or at
enterocolitis, intra-
>34 weeks AOG
ventricular hemorrhage,
oligohydramnios,
renal failure
• Inhibition of
Oxytocin
oxytocin receptors • Maternal: injection-site
receptor • Atosiban
antagonists in myometrium and reaction
decidua
*Somecontraindicationsto tocolyticsincludesevere preeclampsia,placentalabruption,intrauterineinfection,
advancedcervicaldilatation,or evidenceof fetalcompromiseor placentalinsufficiency
Source:ACOG,2016

232
II.STEROIDS
• Antenatal steroids should be given to patients at risk for preterm labor and delivery
between 26 and 34 weeks AOG
• Administration may also be considered in those at risk for preterm delivery >34 weeks to
36 617 weeks provided they were not given a previous course of antenatal steroids
• Regimens:
Betamethasone: 12 mg/IM every 24 hours for 2 doses, OR
• Dexamethasone: 6 mg/IM every 12 hours for 4 doses

III. PROGESTERONE:
• Recall that parturition involves progesterone withdrawal mediated by decreased activity
of progesterone receptors - therefore, giving progesterone may block preterm labor
• 17-Hydroxyprogesterone caproate (17-0HPC) given in weekly 250 mg/IM injections from
16-20 weeks through 36 weeks
• Micronized progesterone: daily 200 mg PO or per vagina (preferred route) from
24-34 weeks AOG
• Counteracts prostaglandin stimulatory activity, decreases myometrial oxytocin receptors
• PO route may cause nausea, headache, and sleepiness

Algorithm for Screening & Treatment of Singleton Pregnancies to Reduce Preterm Birth

~ Singleton gestation with history of ~o

■
l7 spontaneous preterm birth after 16 weeks J

Mutual decision making and risk Cervical length <20 mm

stratification regarding progesterone use
(weekly 17-0HPC injection vs.
Start daily vaginal progesterone capsule
daily vaginal progesterone) starting at
200 mg or gel 90 mg until 36 weeks
16-20 weeks until 36 weeks.

Cervical length measurement Continue weekly cervical length

every 2 weeks from 16 up to 24 weeks measurements

Offer cerclage if Offer cerclage if

Cervical length <25 mm, AND Cervical length continues to shorten
with previous spontaneous up to <1 cm OR
preterm birth at <34 weeks Cervixdilates with membrane exposed

• Cervical length is the best predictor of preterm birth (a history of spontaneous preterm
birth and short cervix are strong risk factors)
• Vaginal progesterone (either in capsular or in gel form), 170HPC, and cerclage can be
used to prevent the reoccurrence and the indications for such interventions should be
individualized
• For those with a short cervix in 2"" trimester without prior history of spontaneous
preterm birth, progesterone is the choice of treatment
• Cervical pessary use is an option, if available
• In multiple gestations, no intervention has been shown to effectively prevent preterm
labor

Source:Li, Chao.Maternal-Fetal
Medicine;
2020

233
IV. OMEGA-3LONGCHAIN POLYUNSATURATEDFATTYACIDS (LCPUFAs)
• Supplementation with Omega-3 LCPUFAs(>l gram per day) can significantly decrease
the risk of preterm delivery
• Best when given <20 weeks AOG
• Theories suggest that Omega-3 LCPUFAsare associated with downregulation of
inflammatory processes in the body by modulating prostaglandin synthesis and inhibiting
palmitate-induced inflammatory cascade leading to prolonged gestation

V. ANTIBIOTICS
• Antibiotics in the management of preterm labor depends on the presence of symptomatic
maternal infections like vaginitis or cervicitis, cystitis or pneumonia
• Antibiotics in idiopathic spontaneous preterm labor without clinical signs and symptoms
of infection does not significantly decrease the incidence ofpreterm birth
• GBSprophylaxis may be given in the following clinical situations:
Previous infant with invasive GBSdisease
GBSbacteriuria during any trimester
0 Positive GBScultures in late gestation during current pregnancy
Unknown GBS status PLUS:
• Preterm labor
• Ruptured membranes 2'18 hours
• lntrapartum temperature 2'39.0 'C
• lntrapartum nucleic acid amplification test (NAAT)positive for GBS

VI. CERCLAGE
• Refers to a variety of procedures to reinforce the cervix during pregnancy in women with
an incompetent cervix
• Offered to patients with prior preterm birth and short cervix (<2.5 cm) on ultrasound
• Approach maybe transvaginal, tranasabdominal or laparoscopic
• Multifilament/braided sutures such as Mersilene is used

PURPOSE I TIMING OF CERCLAGE AND INDICATIONS

Primary • Done at 10-12 weeks AOGin patients previously diagnosed
(Prophylactic) with an incompetent cervix
• Usually done:
Secondary 0 After detection of early cervical changes with no membrane
(Therapeutic) exposure
0 High-risk for preterm delivery (e.g., short cervix <2.5 cm)
Tertiary
• For severe cervical changes with membranes exposed
(Emergency/ Salvage)

VII. CERVICALPESSARY(ARABIN PESSARY)

• Changes the inclination of the cervical canal and compresses the cervix
• The use in prevention of preterm birth in a women with sonongraphically short cervix
may be beneficial to some population

234
PRELABOR RUPTURE OF MEMBRANES (PROM)
• Previously known as premature rupture of membranes
• Refers to the rupture of membranes at ;,,37 weeks AOG,before the onset of uterine
contractions
• Preterm prelabor rupture of membranes (PPROM) refers to the rupture of membranes at
<37 weeks AOG,before the onset of uterine contractions

I. ETIOPATHOGENESIS
A. Pathophysiology
0 Major etiologic factor is the presence of lower tract infection triggering a host-
inflammatory response, leadin to weakness & rupture in chorioamnionic membrane

• Cervicovaginitis • Prior PROM/ preterm delivery

• Incompetent cervix • Prior cervical surgery
• Cigarette smoking • Vaginal bleeding
• Chorionic villous sampling or • Placental pathology
amniocentesis • Male fetus
• Coitus
• Mineral & vitamin deficiency
• Cervical examinations

• Infection
• Prolapse of the umbilical cord
• Premature births
• Prematurity
• Infection
• Respiratory distress syndrome
■
.

(complication of prematurity)
• Umbilical cord compression/prolapse
• Neonatal death

II. MANIFESTATIONS
• Sudden gush of fluid from the vagina, not associated with uterine contractions
• Speculum examination: pooling of amniotic fluid in posterior vaginal wall
• Internal exam: absence of membranes

III. DIAGNOSIS
• A correct diagnosis of PROM is of great importance
False-positive diagnosis may lead to a non-indicated intervention (e.g., early delivery,
surgical delivery)
False-negative diagnosis may place the infant and mother at increased risk of infection
which may be life threatening to one or both

A. Nitrazine Test
0 Amniotic fluid is normally alkaline (pH of 7.0 to 7.5)
0 It is done to determine the nature of vaginal fluid when PROM is suspected
Procedure: This test involves putting a drop of fluid sample from the vagina onto paper
strips containing nitrazine dye. The strips change color depending on the pH of the fluid
Interpretation:
• The strips will turn blue if the pH is greater than 6.0 due to alkalinity of fluid
• A blue strip is suggestive of membrane rupture
• False positive result may be due to contamination with blood, semen, bacterial vaginosis
and cervical secretions

235
 B. Fern Test
0Vaginal secretions are inspected on microscopy for crystallization (i.e., ferning pattern
or arborization)
° Crystallization is due to an increased concentration of protein & electrolytes within fluid
0Vaginal secretions do not show the ferning pattern during pregnancy, but if amniotic
fluid is present, the fern pattern is seen

C. Immunoassays
° Fetal fibronectin
0 Placental alpha-microglobulin-1 (PAMG-1):most reliable method (not locally available)
0 Insulin-like Growth Factor Binding Protein-1 (!GFBP-1): Actim-PROM®1-step dipstick

IV. MANAGEMENT
• Determine the age of gestation by review of history and early ultrasound scan
• Management depends on the age of gestation at the time of rupture
• Patients with PROMwill usually deliver within 48 hours

I <24 WEEKS I 24-31 WEEKS I 32-33 WEEKS I ;,;34WEEKS

• Expectant
• Expectant management • Plan
General management • Expectant • MgSO4 for delivery
approach or induction of management neuro- • Labor
labor protection induction
considered***
GBS • Not
• Yes • Yes • Yes
prophylaxis* recommended
• Yes (up to
Corticosteroids • Considered • Yes • Yes
36 6'' wks)
• To prolong • To prolong
Antimicrobials** • Considered
latency latency
---
Tocolytics • No consensus • No consensus --- ---
'GBS prophylaxis:
ampicillin
2 g IVq6 for48 hours
"Antibiotics
givento prolonglatency:GBSprophylaxis+erythromycin 250mg/IVq6 x 48 hours,then
amoxicillin
250mg/capq8 + erythromycin 500mg/tabq8 x 5 days
"'MgSO,:4 g/SIVin 30 minsthen 1g/hrdripuntildeliveryor max24 hoursifnotdelivered

Expectant Management in Preterm PROM (PPROM)

• Modifiedbed rest
• Periodicmonitoringforinfectionand labor
• Temperature monitoring:T >38°and withuterinetenderness& maternal/fetal
tachycardiais indicative
of infection
• Leukocyte count
• Tocolysisuntilcompletionofantenatalcorticosteroids
• Steroidtherapy:beneficialbetween24 to 32 weeksAOG
• Antibiotic
use: decreaseneonataland maternalmorbidities
Source:ACOG;2016,2017
Cunningham
FG,et al. Williams
Obstetrics;2018

236
INTRAAMNIOTIC INFECTION AND CHORIOAMNIONITIS
I. ETIOPATHOGENESIS
• Term used when clinical findings of infection resulting in
Intraamniotic
inflammation of any combination of the amniotic fluid, placenta,
infection
fetus, fetal membranes, or decidua is present
• Term used to denote histopathologic findings of inflammation of
Chorioamnionitis
the chorion, amnion, and/or umbilical cord

II. CRITERIA FOR DIAGNOSINGCHORIOAMNIONITIS

Any pregnancy at the age of viability with fever 38 °C lasting at least 1 hour; or
One episode of fever >38.3 °C with a history ofat least 1 of the following:
• Ruptured bag of waters
• Prolonged labor
• Multiple internal examinations
PLUS at least 2 of the following criteria:
• Uterine pain • Maternal leukocytosis
• Offensive-smelling discharge • Uterine fundal tenderness
• Maternal tachycardia (>100/min) • Inflammation of placenta, membranes or umbilical
• Fetal tachycardia (>160/min) cord (funisitis) upon histopathologic examination.

■
*Fever is the only reliable clinical indicator of chorioamnionitis
Source:PIDSOGandPOGS,CPGon ObstetricandGynecologic
Infectious
Diseases,
2ndEd;2015

Ill. DIAGNOSTICS
• The following laboratory tests support the diagnosis of intra-amniotic infection:
0Maternal leukocytosis
0Elevated CRP
0In mid-2"' trimester fetal losses, fetal autopsy plus placental biopsy may confirm if
chorioamnionitis was the cause of fetal death

IV. MANAGEMENT
A. General Approach to Prevent Adverse Maternal/Neonatal Sequelae
0 Deliver the baby regardless of age of gestation
Mode of delivery will depend on the usual obstetric indications
0

Give antenatal steroids (if AOG<34 weeks)

0

IV antibiotic therapy started immediately and continued until delivery (> 1 dose
0

postpartum may be given in some cases)

Longer antibiotic therapy for patients who underwent cesarean section and with risks
0

for surgical site infection (obese, prolonged rupture of membranes, prolonged labor)
Administer paracetamol for maternal fever >38°C
0

B. Antibiotic Therapy
0 Benefits of antimicrobial treatment:
• Fewer women developed chorioamnionitis
• Fewer newborns developed sepsis, and
• Pregnancy was more often prolonged for 7 days
REGIMEN
I MANAGEMENT
• Benzylpenicillin (penicillin G) SM units loading dose, then
If with GBS infection or
2.5-3M units IV q4
history ofGBS
• If allergic to penicillin: give clindamycin 900 mg IV q8
For spontaneous • Ampicillin 2 g IV q6 AND
vaginal delivery • Gentamicin 1.5 mg/kg IVq8
• Clindamycin900 mg IVq8 until delivery OR
For Cesarean delivery Metronidazole 500 mg IVq8 AND
• Gentamicin 1.5 mg/kg IVq8
Source:PIDSOGandPOGS,CPGon ObstetricandGynecologic
InfectiousDiseases,2ndEd;2015
Cunningham
FG,et al. WilliamsObstetrics;
2018
237
 SECTION TWO
FETAL DEMISE, POSTTERM PREGNANCY,
AND PROLAPSED CORD

INTRAUTERINE FETAL DEMISE (STILLBIRTH)

• Fetal death in utero (FDU)
• Death prior to complete expulsion/extraction from mother, regardless of the duration of
pregnancy

I. CAUSES OF STILLBIRTHS
• Obstetrical complications (e.g., abruption, ruptured membranes at 20-24 weeks,
multifetal gestation)
• Placental abnormalities (e.g., uteroplacental insufficiency)
• Fetal malformations
• Infection involving the placenta or fetus
• Umbilical cord abnormalities
• Others: hypertensive disorders, diabetes, antiphospholipid antibody syndrome (APAS)

II. MANIFESTATIONS
• Changes noted immediately after fetal death: absent cardiac activity and fetal movement
(on real-time ultrasound findings)
• Suspected with loss of perceived fetal movement and lack of uterine growth
• After 20 weeks, diagnosis is confirmed by ultrasound (before 20 weeks, it is referred to as
an abortion)
ASPECT I CONFIRMATORY FINDING
Heart tones • Not detected by auscultation with a stethoscope or Doppler stethoscope
• Not detected by electronic fetal monitoring using an external
Cardiac activity
sonocardiogram or an internal scalp electrode
• Not detected by real time ultrasound
• There is no cardiac or great vessel vascular motion, which is 100%
Heart motion
accurate in diagnosing fetal demise
• Method of choice

lll. DIAGNOSIS
DIAGNOSTIC
I FINDINGS
• Robert sign (gas in the great vessels): caused by postmortem blood
degeneration
Radiologic • Spalding sign (overlapping skull bones): caused by collapse of the
(x-ray) fetal brain
• Angulation of the fetal spinal curvature: caused by loss of tone of
paraspinal muscles and ligaments

Sonologic • Absence of fetal cardiac and somatic activity

(ultrasound} • Lack of gross body movements, lack of extremity flexion & extension

Amniocentesis • Reveals port-wine-colored amniotic fluid

238
To determine the etiology:
WORK-UP I REMARKS
Infectious • TORCHstudies (fetal infection)
work-up • Listeria culture (fetoplacental infection)
Anticardiolipin Ab/
• Antiphospholipid antibody syndrome (APAS)
lupus anticoagulant
Fetal autopsy • Gross anomalies suggesting a syndrome
Karyotype • Abnormal fetal chromosomes
Total body fetal
• Osteochondrodystrophic disorders
radiograph
Maternal Kleihacuer-
• Fetomaternal bleed
Bettze test
Typical Ab titer • Maternal isoimmunization
75gramOGTT • Maternal diabetes mellitus

IV. MANAGEMENT
• This generally includes expeditious termination of the pregnancy

I
• Labor induction with prostaglandins or high-dose oxytocin if not yet in labor
• Cervical examination should be done to assess if cervix is favorable for labor & delivery
'
A. General Approach
• Labor can be induced, anticipating vaginal delivery
• Artificial rupture of membranes and IV-oxytocin infusion are
Favorable cervix
used to induce labor
• There is no benefit to delivering a dead fetus via cesarean section
• Use of the following should be considered:
Unfavorable cervix • Cervical ripening agents (e.g., dinoprost)
• Laminaria

B. Management of Subsequent Pregnancy after Stillbirth

• Medical and obstetrical history (e.g., evaluation of prior
Preconceptional
stillbirth, determination of recurrence risk)
or initial prenatal
• Counseling: genetic, lifestyle, weight loss for obese patients
visit
• Screening: diabetes, antiphospholipid antibodies (as needed)
• Dating sonography
First trimester • Screening (1st trimester): pregnancy-associated plasma
protein-A, hCG, nuchal translucency
• Fetal sonographic anatomical survey at 18-20 weeks AOG
• Maternal serum screening (quadruple) or single-marker alpha
Second trimester
fetoprotein if first-trimester screening elected
• Possible uterine artery Doppler studies at 22-24 weeks AOG
• Starting at 28 weeks:
• Sonographic screening for fetal-growth restriction
Third trimester • Kick counts (fetal movement counting)
• Antepartum fetal surveillance starting at 32 weeks or 1-2 weeks
earlier than prior stillbirth
• Elective induction at 39 weeks
Delivery • Delivery before 39 weeks only with documented fetal lung
maturity (by amniocentesis)
Source:Reddyet al. ObstetGynecol;2007
Cunningham
FG,et al. WilliamsObstetrics;
2018
239
POSTTERM PREGNANCY
• The terms "postterm", "prolonged", "postdate", & "postmature" are often used to describe
pregnancies that exceeded a duration considered to be the upper limit of normal

I. ETIOPATHOGENESIS
A. Definition of Terms
TERM I DEFINITION
• Pregnancy that goes beyond 42 weeks AOGor greater than 294
Postterm or
days from the first day of the LNMP
prolonged
• Definition assumes that the last menses was followed by ovulation
pregnancy
and fertilization 2 weeks later
• Refers to the specific clinical fetal syndrome in which the newborn
has features indicating a pathologically prolonged pregnancy
Postmaturity • Wrinkled, patchy, peeling skin
syndrome • Long nails
• Long, thin body suggesting wasting
• Open-eyed, unusually alert, and appears old and worried
Source:ACOG,2016

B. Etiology
• Inaccurate aging
• Diminished levels of circulating estrogens (e.g., anencephaly, fetal adrenal hypoplasia,
and fetal pituitary hypoplasia)
• Genetic predisposition
• Irregular ovulation

II. ADVERSE OUTCOMESASSOCIATEDWITH POSTTERM PREGNANCY

A. Adverse Maternal and Perinatal Outcomes
MATERNAL ADVERSE OUTCOMES I PERINATAL ADVERSE OUTCOMES
• Fetal macrosomia (70-80%) • Postmaturity syndrome (20-30%)
• Oligohydramnios • Stillbirth
• Preeclampsia • Meconium aspiration
• CS (due to dystocia, fetal jeopardy) • Birth injuries
• Postpartum hemorrhage
Source:Cunningham
FG,et al. WilliamsObstetrics;
2018

BD tu ·ty S d V M

FEATURES I DYSMATURITY SYNDROME I MAC ROSO MIA

(Weight >4,000-4,500 g)
• Deteriorating (infarction &
Placental function • Maintained
aging)
Amniotic fluid • Decreased • Normal
Neonatal • Scrawning (decreased • Large (increased
appearance subcutaneous tissue) subcutaneous tissue)
Causes of • Cord compression
• Fetopelvic disproportion
increased CS rate • Placental insufficiency
• GIT maturity
Causes of in utero
• Anal sphincter hypotonia • GIT maturity
meconium passage
from acidosis
Causes of • Acidosis
neonatal • Meconium aspiration • Birth trauma
morbidity • Hypoglycemia

240
III. MANAGEMENT
• At 42 weeks -> labor induction
• Consider labor induction at 41 weeks

41 weeks

Uncomplicated With complications

Hypertension
Oligohydramnios
Consider
Fetal surveillance
• Membrane sweeping

42 - 42 617weeks

Labor induction

L. • After completing 42 weeks, recommendations are for labor induction - _,

2016
1·..
·._.
S_o_u_rc-e-:A-C-O-G-,-
_•_l_n_it_i_at_i_o_n_o_f_f_et_a_l_s_u_rv_e_i_ll_a_n_ce_a_t_4_1_w_ee_k_s_is_r_e_a_s_o_n_ab_l_e
________

DATE I MANAGEMENT
IftheAOG is
confirmed, and the
cervix is favorable
lftheAOG is
confirmed, but the
cervix is unfavorable
(Bishop score S4)
If the dates are
questionable
• Labor induction via IV oxytocin after negative contraction
stress test
• Continuous intrapartum fetal monitoring should be performed
while watching for severe variable decelerations from cord
compression and late decelerations from fetal hypoxia
• Cervical priming agent given prior labor induction after
negative contraction stress test
• Continuous intrapartum fetal monitoring should be performed
while watching for severe variable decelerations from cord
compression & late decelerations from fetal hypoxia
• Request for (ultrasound) maturity indices
• Both the NST & AF! can be performed twice weekly while
waiting for spontaneous labor to occur
• Delivery should take place if the NST becomes non-reactive or
if the AF! <S cm

241
UMBILICAL CORD PROLAPSE
• Umbilical cord lies beside or below the presenting part
• Associated with a high fetal mortality rate and carries an increased maternal hazard from
the operative procedures used in treatment

I. ETIOPATHOGENESIS
A. Classification of the Prolapsed Cord
CLASSIFICATION I DESCRIPTION
Umbilical cord
• Membranes are intact
presentation

• Membranes are ruptured

• The cord may occupy three positions:
Umbilical cord
Lie beside the presenting part at the inlet
0
prolapse
Descend into the vagina
0

Pass through the introitus and out of the vagina

0

B. Etiology
0 Whenever the presenting part does not fit closely and fails to fill the inlet of the pelvis,
danger of prolapse of the umbilical cord exists
ETIOLOGY I CAUSES
• Abnormal presentation
• Prematurity
Fetal
• Multiple pregnancy
• Polyhydramnios
• Long cord
Cord and Placenta
• Low-lying placenta
• Artificial rupture of the membranes
• Disengaging the head
Iatrogenic
• Flexion of an extended head
• Version and extraction

II. DIAGNOSIS OF UMBILICAL CORD PROLAPSE

• Since the fetal mortality is high once the cord has protruded through the introitus, earlier
means of diagnosis must be sought
• Diagnosis of prolapse of the cord is made in two ways:
0 Visualization of the cord within the vaginal canal
0 Palpation of the cord on internal examination

III. MANAGEMENT OF UMBILICAL CORD PROLAPSE

A. Immediate Delivery of the infant is the Optimal Treatment, EXCEPT WHEN THE
FETUS IS:
0 Dead
, Known to have fatal anomalies (e.g., anencephaly)
, Premature that has lesser chances of survival

B. Temporary Measures
0 Aim to lessen compression of the umbilical cord by:
• Push the presenting part up and away from the cord
• Place the patient in the knee-chest or Trendelenburg position, with the hips
elevated and the head low
• Oxygen support by mask is given to the patient
• Check fetal heart rate via transabdominal auscultation or palpation of the
umbilical cord
• Ascertain presentation, cervical dilatation, station of the presenting part, and
condition of the cord through vaginal examination
• Tocolytic drug can be given in an intravenous infusion to reduce pressure on the
umbilical cord from uterine contractions
242
C. Cervix Fully Dilated
° Cesarean section (CS) is the best treatment if it can be performed without delay
0 If CS cannot be carried out immediately the following procedures are indicated and
may be performed, as long as an experienced operator is available:

Cephalic • Internal podalic version and complete breech extraction

presentation, There is the danger of rupturing the uterus, but since this is a
Head HIGH desperate attempt to save the child, the chance is taken
Cephalic
• Extraction by forceps
presentation,
• Highly operator-dependent
Head LOW
Breech
• Extraction as a footling breech
presentation
• Internal podalic version to convert into a footling breech
Transverse Lie
presentation and immediate complete breech extraction

D. Cervix Incompletely Dilated

0Immediate Cesarean delivery
0Repositioning of the cord may be attempted if Cesarean section cannot be performed

I
.

243
 SECTION THREE
MULTIPLE GESTATIONS
MULTIPLE GESTATION
• Fueled largely by infertility therapy, rate and number of multifetal births increased
dramatically
• These rates of multifetal pregnancies may be associated with maternal and fetal complications

I. ETIOLOGIES
• Twin fetuses usually result from:
° Fertilization of two separate ova, which yields dizygotic or fraternal twins; or
° Fertilization of a single ovum that then divides to create monozygotic or identical
twins (less often)
• Mechanisms differentiating dizygotic and monozygotic twin pregnancy are as follows:

I DlZYGOTIC I MONOZYGOTIC
Also known • Double ovum, dizygotic or fraternal • Single ovum, monozygotic or
as twins identical twins
• Twins resulting from fertilization of • Twins arising from a single
two ova during a single ovulatory fertilized ovum that subsequently
Description cycle ( e.g., each twin will have its divides into two similar structures,
own chorion and amnion and two each with a potential to develop
placentas) into a separate individual
Fertilization • 2 sperms + 2 eggs • 1 sperm + 1 egg
Genetic
• Different between twins • Same between twins
make-up
FetaISex • Same or different sex • Same sex
• Depends on the time of division
Membranes • Dichorionic-diamnionic
(see table on next page)
Placenta • One fused or two separate • One or two
Incidence • Depends on race, heredity, age, parity • Constant (1 per 250 pregnancies)

II. SPECIALCASES IN MULTIPLEGESTATIONS

EVENT I REMARKS
• An interval as long as one or longer than one ovulatory cycle
Superfetation intervenes between fertilizations
• Another conception occurring during an established pregnancy

Superfecundation • Fertilization of two ova within a period of time, but not at the same
coitus nor necessarily by sperms from the same partner
• Improved ultrasound technique can now detect twins early in the
1st trimester, allowing documentation of the absorption of an early
Vanishing Twin
fetal demise of a second of twin
• Incidence of twins is more during the first trimester, than at term
• A term used in obstetric imaging to describe a significant size or
weight difference between the two fetuses of a twin pregnancy
Twin
• Birth weight discordance= (larger twin weight• smaller twin weight)
Discordancy
larger twin weight x 100
• A discordancy of>25% is considered significant
Twin-to-Twin • Blood is transfused from the donor twin to its recipient
Transfusion • Donor becomes anemic and the recipient becomes polycythemic
syndrome • Significant mortality (70%) of one or both twins if left untreated
244
III. GENESIS OF MONOZYGOTICTWINS
• The outcome of the monozygotic t:\vinning process highly depends on the timing of division
• Sonographic determination of chorionicity is considered a recognized indication for first-

I I
trimester sonography

TIME OF
DIVISION I EVENTS
OCCURING OUTCOME ILLUSTRATION

amnion chorion
• Diamnionic,
dichorionic,
• Division occurs
monozygotic
before the inner
twins
1" 72 cell mass (morula)
• Two embryos
hours from is formed and
each in separate
fertilization outer layer of
amnionic and
blastocyst is not
chorionic sac
yet the chorion
• Placenta may be
t:\Vo or fused

• Diamnionic,
monochorionic,
• Division occurs
monozygotic
after the inner cell
4'"to 8 th
day from
fertilization
mass is formed
and cells destined
to be the chorion
has differentiated,
but those to be the
t\Vins
• Two embryos,
each in a separate
amnionic sac,
both covered
I
.

by a common
amnion have not
chorion & share a
placenta

chorion

• Monoamnionic,
monochorionic,
monozygotic
• Chorion t\Vins
8 th to 12 th
and amnion • Two embryos
day from
have already within a
fertilization
differentiated common
amnionic sac
and chorion and
share a placenta

• Cleavage is
incomplete
• Division occurs • Conjoined
After 12
when the embryos within
days from
embryonic disk is a common
fertilization
formed amnionic sac
and chorion and
share a placenta

Terminologies:
• Diamnionic:
twoseparate
amnionicsacs(innersac) • Monoamnionic:
oneamnionicsac
• Dichorionic:
twoseparate
chorionic
sacs(outersac) • Monochorionic:
onechorionic
sac
245
IV. ANTEPARTUM MANAGEMENT OF TWIN PREGNANCIES
A. Complications

FETAL I MATERNAL

• Spontaneous pregnancy loss • Preeclampsia

• Higher rates of chromosomal and • Abruptio placenta
congenital anomalies • Thrombocytopenia
• Fetal growth restriction • Acute fatty liver
• Discordant growth of twins • Gestational diabetes mellitus
• Single fetal demise • Postpartum hysterectomy
• Twin-to-twin transfusion syndrome
(specific for monochorionic gestations)
• Preterm Birth

B. Goals of Twin Pregnancy Antepartum Management

0 Determine chorionicity by sonography during the first trimester
0 Prevent markedly preterm delivery
0 Identify failure of one or both fetuses to thrive so delivery can be planned before they
become moribund
0 Avoid fetal trauma during labor and delivery
0 Provide expert neonatal care

C. Aspects of Twin Pregnancy Antepartum Management

0 Plan as soon as pregnancy is detected; close monitoring is continued throughout
pregnancy
0 Determine the chorionicity and amnionicity for risk stratification
0 Additional nutritional requirements & supplementation should also be given to
support the pregnancy
0 Below is a summarized antenatal guideline for higher order gestations:
ASPECT
I REMARKS

• Additional 300 kcal/day

• Extra supplementation above that supplied by a prenatal vitamin
Diet includes folic acid 1 mg/day and Iron 60 mg/day
• Low-dose aspirin started between 12-28 weeks AOGto reduce risk
of preeclampsia, preterm birth and fetal growth restriction.
• Ultrasound is performed in the 1st trimester to assess viability,
gestational age and chorionicity.
Antepartum • Serial growth assessment may be done every 4 weeks from 18
Surveillance weeks until delivery
• If with growth discordance or intrauterine growth restriction,
manage same as singleton pregnancy
• Transvaginal cervical length (CL) performed between 18-24 weeks
Prediction of • Bed rest and tocolytic agents are not effective
Preterm Birth • Corticosteroid use as in singleton guideline
• Progesterone therapy given for shortened cervix
• Hypertension occurs earlier in multiple pregnancy
Maternal • Maternal anemia
Co-morbidities • Other medical co-morbidities should be checked and managed
same as in singleton pregnancy
PPROM • Expectant management but may go into spontaneous labor earlier

246
V. INTRAPARTUM MANAGEMENT OF TWIN PREGNANCIES
A. Timing of Delivery
° Chorionicity and amnionicity of otherwise uncomplicated twin pregnancies determine
the timing of delivery
0 Below is a summary of suggested timing of delivery based on the chorionicity and
complications present in twin pregnancy:

TYPE OF TWIN PREGNANCY I SUGGESTED TIMING

OF DELIVERY*
Dichorionic-diamnionic twins, uncomplicated • 37 to 37 6'' weeks
Monochorionic-diamnionic twins, uncomplicated • 34 to 37 617 weeks
Monoamnionic-monochorionic twin, uncomplicated • 32 to 33 6'' weeks
Monochorionic-diamnionic with one growth restricted twin
• 36 to 36''' weeks
with normal umbilical artery Doppler
Dichorionic-diamnionic twins with one growth restricted twin
• 34 to 34''' weeks
with abnormal umbilical artery Doppler
Monochorionic-diamnionic twins with one growth restricted
• 32 to 33''' weeks
twin with absent umbilical artery Doppler
Dichorionic-diamnionic twins with one growth restricted twin
with absent umbilical artery Doppler • 30 to 31 6'' weeks

Dichorionic-diamnionic twins complicated by maternal morbidity

Monochorionic-diamnionic twins with one growth restricted twin
According
to theAGOG(2016),recommended deliverytimesare simplified
as follows:
• 32 to 34 6' 7 weeks
• 32 to 34 6'' weeks
I
.

• Uncomplicated
dichorionic
twins:38 weeks
• Uncomplicated
monochorionic twins:between34 and37 6n weeks
diamnionic
• Monoamnionictwins:32to 34 weeks
Source:BerghellaMaternal-Fetal
EvidenceBasedGuidelines,
Chapteron Multifetal
Pregnancy,3rdedition
AGOG;2016

B. Twin Pregnancy Presentation

0Positions and presentations are best confirmed sonographically
0Most common presentations at admission for delivery are:
• Cephalic-Cephalic (42%)
• Cephalic-Breech (27%)
• Cephalic-Transverse (18%)

C. Route of Delivery
0 Time interval of delivery between the first and the second of twin has no clinical
significance, but the remaining twin must be monitored closely
TYPE OF PREGNANCY
I ROUTE OF DELIVERY*
Monoamnionic-
monochorionic twin
• Cesarean delivery
If twin A is malpresented
Both twins are malpresented
• With EFW 1500-3500 g: may allow vaginal delivery**
Twin B is malpresented
• With EFW <1500 g: consider Cesarean delivery
Both cephalic presentation • May allow vaginal delivery
'In general,cephalicpresentation
ofthefirstfetusinlaboringwomenwithtwinsmaybe consideredforvaginaldelivery
"Vaginaldeliveryonlyperformed byan experienced obstetrician
oroperator,
withadequateanesthesia/analgesia
Source:AGOG;2016

247
 SECTION FOUR
FETAL GROWTH DISORDER
FETAL GROWTH RESTRICTION (FGR)
I. ETIOPATHOGENESIS
• Compromised uteroplacental perfusion
• Fetus redirects blood flow to more vital organs
• This pattern of redistribution may be evident by a decreased diastolic flow in the
Umbilical artery Doppler studies
• Body fat, lean mass, and bone mineral content are reduced

A. Definition of Terms
1. Intrauterine Growth Restriction (IUGR)
• Term used to describe the size of the fetus in-utero
• Not synonymous to small for gestational age (SGA)
• EFW <10th percentile because of a pathologic process
• Diminished growth velocity documented by at least 2 intrauterine growth assessment
usually associated with abnormal Doppler findings of the umbilical arteries

TYPE
I DEFINITION

Early versus Laf/? Onset IUGR

- ·-
• <32 weeks
Early onset • May be due to chromosomal abnormalities, maternal diseases, and/or
IUGR severe placental problems
• With high resistance to flow in the umbilical arteries
• >32 weeks (often >36 weeks)
• May be due to infection, environmental factors, exposure to alcohol/
Late onset
smoking/drugs
IUGR
• May have normal Doppler studies for uterine and umbilical arteries but
with abnormal MCADopplers
Symmetri5;a/ ve~sus Asymmetrical IUGR
-
• "Proportionately" small (i.e., proportionate reduction of both head &
body size)
• Early insult leads to a reduced cell number & size
.Symmetrical • Normal, genetically determined small stature
JUGR • Proportionately small: occurs early with proportionate stunting in length,
weight, and head circumference (all parameters at <lO'h percentile)
• Likely due to intrinsic growth problems (aneuploidy, syndromes,
congenital infections)
• Disproportionarelylaggingabdominal growth compared with the head growth
• Late insult leads to reduced cell size (and not the number)
• Reduced abdominal circumference (AC),which reflects liver size
• Brain sparing IUGR*
Asymmetrical
• Disproportionate stunting in length and weight, in relation to head
JUGR
circumference (HC)
• HC remains appropriate for aging due to "brain sparing"•
• Caused by extrinsic growth problems (e.g., placental insufficiency in the
3rd trimester)
'Brain sparing:normalbrain& head growthbecause of preferentialshuntingof oxygen& nutrientsto the brain

2. Small for Gestational Age

• A term used to describe the size of the baby at birth, usually characterized by either:
• Body weight (BW) lower than a predetermined cut-off regardless of cause; or
• BW 2 SD below the mean or the 10th percentile of a population specific BW vs a
gestational age plot
• May be constitutionally small or small due to intrauterine growth restriction (lUGR)
• Severely SGA: EFW or abdominal circumference less than 3rd percentile
248
 3. Constitutionally Small
• Neonate with BW <10th percentile for gestational age with a normal growth trajectory,
normal Doppler of the umbilical arteries, and normal amniotic fluid volume
• Appropriate size in terms of maternal characteristics
• Less likely to develop any fetal and perinatal complications

B. Causes and Risk Factors of Impaired Fetal Growth

CATEGORY I CAUSES

• Genetic abnormalities
• Aneuploidy
• Fetal infection [cytomegalovirus, toxoplasmosis, rubella, malaria, herpes
Fetus
simplex virus)
• Structural anomaly
• Multiple gestation
• Abruption
• Confined placental mosaicism
Placenta • Placenta accrete syndromes
• Chorioangioma
• Implantation abnormalities
• Maternal low prepregnancy weight, poor gestational weight gain,
malabsorption, poor nutritional status

I
• Short interpregnancy interval
• Extremes of maternal age
• Medical and obstetric conditions .
0Preeclampsia Uterine malformations
0

0Placental abruption Use of alcohol, cigarettes, and/or

0

° Chronic hypertension drugs (e.g., heroin, cocaine)

° Chronic kidney disease Pre-pregnancy radiation therapy
0

Maternal 0Pregestational diabetes mellitus to the pelvis

0Systemic lupus erythematosus Heavy first trimester antepartum
0

0Antiphospholipid syndrome bleeding

° Cyanotic heart disease Previous SGAbaby
0

° Chronic pulmonary disease Previous stillbirth (unless

0

0Severe chronic anemia placental insufficiency was

0Sickle cell disease excluded)
• Living at high altitudes
• Low socioeconomic status
• Race

• Assisted reproductive technologies

Others
• Teratogens/environmental factors

Source:WellmannHA,et al. HormRes. 1998

CunninghamFG,et al. Williamsobslelrics;2018

II. MANIFESTATIONS AND DIAGNOSIS

• Diagnosis is based on discrepancies between actual and expected sonographic biometric
measurements for a given gestational age:
Suspect IUGR if fundic height is 3 cm less than expected
Sonographic EFWt is <lO'h percentile for gestational age on a standardized population
growth curve
Ultrasound with Doppler studies is most effective in differentiating between pathologic
IUGR and a constitutionally small fetus.

Ill. MANAGEMENT
• Review risk factors
• Evaluation of fetal anatomy, placenta, amniotic fluid ultrasound
• Assessment of the umbilical artery by Doppler
• Timing of delivery is individualized on the basis of established gestational age, Doppler
velocimetry studies, growth and biophysical testing

249
FETAL MACROSOMIA
• Macrosomia is defined as birthweights that exceed certain percentiles for a given population)
• Macrosomia is frequently defined based on mathematical distributions ofbirthweight
(see below)

I. ETIOPATHOGENESIS
• 5-10% are associated with maternal diabetes
• Fetal release of insulin, insulin-like growth factors, and growth hormone leads to
increased fetal fat deposition and, in turn, enhanced fetal size

A. Definition of Terms
Large for Gestational • Defined as a weight, length, or HC that lies above the 90th
Age (LGA) percentile for AOG
• BW ;,4,000 g irrespective of AOGor >90th percentile for a given
AOGafter correcting for neonatal sex and ethnicity
Macrosomia 0 Grade I: BW = 4000-4499 grams

0 Grade II: BW = 4500-4999 grams

0 Grade Ill: BW >5000 grams

B. Risk Factors for Macrosomia

0 Genetics (e.g., syndromes, race, and ethnicity)
, Maternal GDM
0 Obesity & excessive weight gain in pregnancy (strongest predictors for macrosomia)
0 History of previous macrosomic babies
° Fetal sex (male> female)
0 Maternal age ;,35 years old
, Excessive amniotic fluid ;e60th percentile
, Grand multiparity (GS and above)
0 Prolonged pregnancy
II. MANIFESTATIONAND CONSEQUENCES

MAJOR SYNDROMES
ASSOCIATED WITH MACROSOMIA
I MAJOR COMPLICATIONS OF
FETAL MACROSOMIA
• Pallister-Killian • Simpson-Golabi-Behmel • Increased risk of CS
• Weaver • Costello • Shoulder dystocia
• Sotos • Beckwith-Wiedemann • Clavicular fracture and damage
• Perlman • Macrocephaly-cutis marmorata • Brachia! plexus injury
• Berardinelli telangiectasia congenita (M-CMTC)
lipodystropia

III. DIAGNOSIS
• Ultrasound: abdominal circumference (AC) >35 cm is the most common and reliable
single UTZ parameter to assess risk of macrosomia
• Because current methods fail to accurately estimate fetal size, macrosomia cannot be
definitively diagnosed until delivery

IV. MANAGEMENT
• When macrosomia is suspected, pregnancy should be classified into uncomplicated,
gestational diabetes, prior cesarean delivery or history of shoulder dystocia
CLASSIFICATION
I MANAGEMENT

Uncomplicated • Consider induction of labor between 37 to 39 617 weeks

• Consider induction of labor between 38 to 38 617weeks

Maternal diabetes
• Elective CS if EFW ;,4000 grams
Prior cesarean • Individualization and patient counseling
delivery • Consider repeat cesarean delivery ifVBACsuccess is unlikely
Prior shoulder
• Consider offering planned primary CS between 39 to 39''' weeks
dystocia
POGS CPG in Felal GrowthDisordersand Abnormahliesin Amniol1c
FluidVolume,November2015
250
 SECTION FIVE
ABNORMALITIES IN AMNIOTIC FLUID VOLUME

OVERVIEW OF AMNIOTIC FLUID VOLUME

I. PHYSIOLOGY OF AMNIOTIC FLUID VOLUME (AFV)
• AFV increases from ~30 mL at 10 weeks to 800 mL by the mid 3rd trimester
• Four pathways play a major role in amniotic fluid regulation:

....

• Fetal lung fluid secretion

'Oligohydramnios: abnormallydecreasedfluidvolume(e.g.,can be causedby uteroplacentalinsufficiency,
which
can reducefetalurineoutput)
0
Polyhydramnios or hydramnios:
abnormallyincreasedfluidvolume(e.g.,can be causedby impairedfetal
swallowingor GI tractobstruction)
Source:MagannEF,et al. ObstetGynecol;1997
CunninghamFG,et al. WilliamsObstetrics;2018

■
II. ASSESSMENT OF AFV
• AFV is routinely assessed during pregnancy because it is a marker of fetal health
• Qualitative or semiquantitative assessment of AFV is a standard component of every 2nd .
and 3rd trimester ultrasound examination
• Volume of amniotic fluid reflects the balance between "fluid production" and "fluid
movement out of amniotic sac"

Ill. ULTRASOUND ESTIMATION OF AFV

A. Qualitative Assessment
Refers to subjective assessment by sonographer, without sonographic
0 measurement
Reported as: oligohydramnios, normal, or polyhydramnios
0

B. Semiquantitative Analysis

PARAMETER I REMARKS
I INTERPRETATION

• Also known as the maximum vertical

pocket (MVP)
Single • Oligohydramnios: SOP 52 cm
• Vertical dimension [in cm) of the largest
deepest • Polyhydramnios: SOP ;e8
pocket of amniotic fluid (not persistently
pocket (SDP) • Normal: between 2 and 8 cm
containing fetal extremities or umbilical
cord
• Calculated by dividing uterus into
Amniotic quadrants • Oligohydramnios: AF! 55 cm
fluid index • AFI is equal to the sum of the maximal • Polyhydramnios: AF! e,24
(AFI) vertical amniotic fluid pocket diamete_r in • Normal: between 5 and 24 cm
each quadrant (in cm)
Source:MagannE, RossMG.Assessment
of amnioticfluidvolume.https://www.uptodate.com/contents/

251
POLYHYDRAMNIOS (HYDRAMNIOS)
• Refers to an excessive volume of amniotic fluid
• Associated with an increased risk of adverse outcomes (e.g., preterm birth, placental
abruption, fetal anomalies)
• Generally from decreased fetal swallowing/diminished absorption or increased fetal
excretion of fluid

I. ETIOPATHOGENESIS
MECHANISM I EXAMPLES/REMARKS
Fetal (Congenital) 1Anom~alies(Structural Abnormalities or Genetic Syndromes)
Impaired • CNS anomaly: anencephaly, holoprosencephaly
swallowing • Craniofacial anomaly: cleft lip/palate, micrognathia
GIobstruction • Esophageal/duodenal atresia
Renaldisorders • Ureteropelvic junction obstruction (paradoxical), fetal Bartter syndrome
Other Causes JI
Increased • Maternal diabetes mellitus causes fetal polyuria from hyperglycemia
urine output and increased osmotic diuresis
(UO) • Fetal anemia can cause increased UO from increased cardiac output
Increased
transudation
• Placental tumors (e.g., chorioangioma)
from enlarged
vessels
• Fetal hydrops
• Congenital viral infection (e.g., TORCH)
Others
• Multiple gestation (e.g., twin-to-twin transfusion)
• Idiopathic
Source:BelooseskyR, Ross MG.Polyhydramnios:
etiology,diagnosis,and management.UptoDate
CunninghamFG,et al. WilliamsObstetrics;2018

II. MANIFESTATIONS
A. Presentation
Hydramnios is suspected if uterine size is large for gestational age (fundal height
0

exceeds the weeks of gestation by >3)

Uterus may feel tense
0

Difficult to palpate fetal small parts or auscultate fetal heart tones

0

Diagnosed during a prenatal ultrasound examination

0

B. Complications
° Fetal anomalies
0 Preterm birth and PROM
0 Macrosomia
0 Malpresentation

° Cord prolapse
0 Abruptio placenta
0 Increased primary CS rate
0 Uterine atony

0 Poor APGAR Score

0 Increased risk of neonatal intensive care unit (NlCU) admission

252
III. DIAGNOSIS
A. Ultrasound Criteria

Mild* • 8 to 9.9 cm • 25 to 29.9 cm

Moderate • 10 to 11.9 cm • 30 to 34.9 cm
Severe • 2:12 cm • 2:35 cm
'Mildhydramnios is the mostcommon.It is frequently andbenign
idiopathic
accordingto the POGS2015CPG
"Classifications
• Mild:8-11cm
• Moderate:12-15cm
• Severe:>16cm
Obstetrics;2018
FG,et al. Williams
Source:Cunningham
POGSCPGin FetalGrowthDisordersandAbnormalities FluidVolume,November
inAmniotic 2015

B. To Determine the Cause

° Congenital anomaly scan
° Fetal karyotyping
TORCHscreening

■
0

0 75gOGTT
.
IV. MANAGEMENT
• Treatment is directed to the underlying cause
• Severe hydramnios may result in early preterm labor or maternal respiratory
compromise. for which amnioreduction (i.e., large-volume amniocentesis) may be needed
AOG I SEVERITY I ANTENATAL SURVEILLANCE
• AFI <30 cm • AFI or SOP every 2-3 weeks
• AFI or SOP weekly to rule our hydrops
• AFI 2:30 cm • Weekly NST or Biophysical profile
23 to 38 6 17 • Consider amniocentesis
weeks
• AFI 2:35 cm • Amnioreduction to normalize AFV
• SOP 2:12 cm • NSAIDtherapy: indomethacin 75-200 mg per day given
• Maternal for 48 hours at <32 weeks AOG
symptoms • Antenatal monitoring beginning at diagnosis or 28 weeks
• Induction of labor and delivery with cautious amniotomy
.?39weeks for idiopathic polyhydramnios
• Cesarean delivery for obstetrical indications only

253
OLIGOHYDRAMNIOS
• Refers to amniotic fluid that is less than expected for gestational age, diagnosed by
ultrasound examination
• Anhydramnios refer to no measurable pocket of amniotic fluid
• Associated with an increased risk for fetal/neonatal death

I. ETIOPATHOGENESIS
• Pregnancies complicated by oligohydramnios include those in which:
AFV has been severely reduced since early 2nd trimester (i.e., fetal abnormality that
precludes normal urination or placental abnormality that impairs perfusion)
AFV was normal until near-term or even full-term (i.e., placental abnormality,
preeclampsia, maternal vascular disease)
• Ruptured membranes should be excluded
Common Etiologies of Oligohydramnios
• Congenital abnormalities, especially those with impaired urine production*
• Isolated/idiopathic form
• Uteroplacental insufficiency**
• Pulmonary hypoplasia
• Complication of multiple pregnancies (e.g., twin-to-twin transfusion)
• Iatrogenic (e.g. postchorionic villous sampling, exposure to ACE inhibitors & NSAIDs)

•sy the2ndtrimester,fetalurinebeginsto entertheamnioticsacandthefetusbeginsto swallowamnioticfluid.

Disordersrelatedto fetalurinarysystemhasa majorrolein etiologystartingthistime
.. Oligohydramnios
firstdiagnosed with uteroplacental
in the3rdtrimesteris oftenassociated insufficiency
(e.g.,
preeclampsia,maternalconditions)

Source:Beloosesky
R, RossMG.Oligohydramnios:
etiology,diagnosis,andmanagement.
UptoDate

II. MANIFESTATIONS
A. Presentation
0 Oligohydramnios first suspected because uterine size (estimated by the fundic height)
is less than expected for AOG

B. Complications

During 1"
• Spontaneous abortion
trimester
• Fetal/neonatal death
During 2 nd • Preterm delivery
trimester • Anatomical & functional abnormalities (e.g. skeletal deformations,
contractures, and pulmonary hypoplasia
• Umbilical cord compression
During 3,• • Uteroplacental insufficiency
• Meconi um aspiration
trimester
• Low BW
• CS for non-reassuring fetal heart rate patterns

254
III. DIAGNOSIS
• Sonographic diagnosis (ultrasound criteria) of oligohydramnios is based on:
, SOP s2 cm (diagnostic method of choice), or
, AFI <5 cm
Source:AGOG,2016

IV. MANAGEMENT

.
• Question woman concerning PPROM
h Id d ocument norma Heta I k'd
Ultrasoun d SOU 1 nevs, bl a dd er, stomac h b u bbl e & ~eta we1g1
ht
• Amnioinfusion: if oligohydramnios (without PPROM) is detected just
before or in labor near or at term
Methods for • Maternal hydration:
increasing AFI ' IV hydration: Intravenous hypotonic versus isotonic solution
' Oral hydration: equally effective as IV hydration (allow mother
to drink 2 liters then reassess amniotic fluid)
• Trial of maternal hydration
Preterm
• If with persistent oligohydramnios, intensive surveillance (non-
with isolated
stress test plus SOP twice weekly) & delivery if with NRFS, abnormal
oligohydramnios
or biophysical profile
Term with • If BPS is reassuring, consider maternal hydration then repeat testing
isolated • With persistent oligohydramnios, consider labor induction versus
oligohydramnios expectant management with 2x weekly fetal surveillance

REFERENCES
I.American College of Obstetricians and Gynecologists: Intrapartum management of intraamniotic infection. Committee
■
'

Opinion No. 712, August 2017

2.American College of Obstetricians and Gynecologists: Mu\tifetal gestations: twin, triplets, and higher-order multifetal
pregnancies. Practice Bulletin No. 169, October 2016, Reaffirmed 2016
3.American College of Obstetricians and Gynecologists: Ultrasound in pregnancy. Practice Bulletin No. 175, December 2016
4.Committee on Practice Bulletins-Obstetrics. The American College of Obstetricians and Gynecologists. Practice Bulletin:
Prediction and Prevention of Preterm Birth. Obstet Gynecol 2012, 120:964
5.Cunningham FG,et al. Williams obstetrics; 2018
6.Li, Chao. Risk Assessment and Prevention of Spontaneous Preterm Birth, Maternal-Fetal Medicine: April 2020 - Volume
2 - Issue 2 - p 89-94
7.Lockwood, Berghelia. Preterm Labor: Clinical findings, diagnostic evaluation, and initial treatment. UpToDate. May 2019.
8.MagannEF.BassJD,ChauhanSP,et al: Amnioticfluidvolume in nonnal singleton pregnancies.Obstet Gynecol90( 4):524, 1997
9.PIDSOGand POGS,CPGon Obstetric and GynecologicInfectious Diseases, 2nd Ed: 2015
10. POGS CPG in Fetal Growth Disorders and Abnormalities in Amniotic Fluid Volume, November 2015
11. Raju TN, Mercer BM, Burchfield DJ,et al: Periviable birth: executive summary of a joint workshop by the Eunice Kennedy
Shriver National Institute of Child Health and Human Development, Society for Maternal- Fetal Medicine, American
Academy of Pediatrics, and American College of Obstetricians and Gynecologists. Obstet Gynecol 123(5):1083, 2014
12. Reddy UM: Prediction and prevention of recurrent stillbirth. Obstet Gynecol 110:1151, 2007
13. Society for Maternal-Fetal Medicine (SMFM) Publications Committee. The choice of progestogen for the prevention of
preterm birth in women with singleton pregnancy and prior preterm birth. American Journal of Obstetrics and Gynecology
2017:216:B11
14. Society for Maternal-Fetal Medicine Consult Series #52: Diagnosis and management of fetal growth restriction, Ami Obstet
GynecolVol223, Issue 4, May2020
15. Wollmann HAIntrauterine growth restriction: definition and etiology.Horm Res. 1998;49 Suppl 2:1.

255
MEDICAL
ISSUES
INPREGNANCY
 SECTION ONE
OVERVIEW OF THE MEDICAL ISSUES IN PREGNANCY

GENERAL CONSIDERATIONS
• A pregnant woman is predisposed to the medical disorders that affect any woman of
child-bearing age
• Pregnancy-induced alterations in virtually all organ systems can amplify the existing
medical condition
• Conversely, the medical condition itself can affect the maternal physiological response to
pregnancy
• Obstetricians should have a working knowledge of the medical disorders common to
women of reproductive age

I. MEDICATIONS
• Most medications in the frequently encountered illness complicating pregnancy can be
safely given
• Some medications that have significant risk to the developing embryo/fetus include:

Some Tera tog ens and Fetotoxic Agents

• Alcohol, tobacco • Paroxetine
• Efavirenz
• ACE inhibitors • Phenobarbital
• Fluconazole
• Angiotensin-receptor • Phenytoin
• lsotretinoin/Tretinoin
blockers • Radioactive iodine
• Lamotrigine
• Androgens • Ribavirin

■
• Lead
• Bosentan • Tamoxifen
• Leflunomide, lenalidomide
• Carbamazepine • Tetracycline
• Lithium
• Chloramphenicol • Thalidomide
• Methimazole
• Cocaine • Toluene
• Mercury
• Corticosteroids • Topiramate
• Methotrexate
• Cyclophosphamide • Trastuzumab
• Misoprostol
• Danazol • Valproic acid
• Mycophenolate
• Diethylstilbestrol (DES) • Warfarin
Source:CunninghamFG,et al. W1ll1ams
Obstetrics;2018

II. RADIOGRAPHY
• Imaging modalities are used for the diagnosis and therapy during pregnancy (e.g.,
sonography, radiography, magnetic resonance imaging)
• Most diagnostic radiographic procedures are associated with minimal fetal risks, so some
guidelines would recommend to limit exposure through radiation safety practices

American College of Obstetricians and Gynecologist Guidelines:

• Sonography and magnetic resonance (MR) imaging are not associated with fetal risks and
are preferred options for imaging in pregnancy
• Radiation exposure during radiography, computed tomography (CT), or nuclear imaging
delivers a lower dose than that associated with fetal harm. If needed to supplement
sonography or MR imaging (or if more readily available), these should not be withheld
• Gadolinium contrast with MRI should be restricted unless it significantly improves
diagnostic accuracy to benefit outcomes
Source.AGOG,2017

259
COMMON
CONCERNS
INPREGNANCY
CONDITION
I REMARKS
I REMEDY/MANAGEMENT
• Persists until 14-16 weeks AOG • Vitamin B6, doxylamine,
• Hyperemesis gravidarum: severe phenothiazine or Hl-receptor
Nausea and
vomiting causing dehydration, blocking antiemetics
vomiting
electrolyte & acid-base • Eating small meals at frequent
disturbances & starvation ketosis intervals
• Periodic rest with leg elevation, elastic
stockings
• Lower extremities varicosities • Surgery (injection, ligation or
stripping of veins) during pregnancy
generally is not advised unless severe
Varicosities • Fitted pantyhose, foam rubber pad
and • Vulvar varicosities suspended across the vulva by a belt
hemorrhoids to exert pressure on the dilated veins
• Topical anesthetics, hot sitz bath, and
stool-softening agents
• Hemorrhoids • Incision & removal of the clot under
local analgesia for thrombosed
external hemorrhoids
• Due to exagerrated lordosis • Reduced by squatting rather than
in pregnancy, exacerbated by bending when reaching down, using a
Backache
significant bending, lifting, or pillow back support when sitting and
walking by avoiding high-heeled shoes
• Results from upward • Small frequent meals & avoidance of
displacement and compression bending over or lying flat
Heartburn of the stomach by the uterus, • Antacids, aluminum hydroxide,
combined with relaxation of the magnesium trisilicate, or magnesium
lower esophageal sphincter hydroxide alone or in combination
• Craving for strange food
0 Pagophagia: craving for
nonfoods such as ice • Maintain a healthy, balanced diet
0 Amylophagia: craving for • Take prenatal multivitamins & iron
Pica
starch daily
0 Geophagia: craving for clay • Resist intake of non-food items
• May be triggered by severe iron
deficiency
• Eating small frequent meals
• Salivation sometimes appears to
• Chewing gum or sucking hard candies
Ptyalism follow salivary gland stimulation
• Taking small, frequent sips of water
by ingestion of starch
• Rinsing mouth frequently

Sleepiness • Daytime naps

• Progesterone has a soporific
and fatigue • Mild sedatives at bedtime, if due to
effect
insomia

• Normal increase of vaginal

discharge due to increased
• Regular daily hygiene
secretion by cervical glands due
• Use panty-liners as needed
Leukorrhea to hyperestrogenemia
• Treat superimposed infections if any
• Pathologic due to vulvovaginal
infections (e.g.,bacterial vaginosis,
candidiasis or trichomoniasis)
Source:SuzukiS, et al. NorthAmericanJournalof MedicalSciences;2009
ThaxterNesbethKA,et al. EuropeanJournalof Obstetrics, Gynaecology& Reproductive Biology;2018
Cunningham FG,et.al.WilliamsObstetrics25thEdition.2018
260
 SECTION TWO
HYPERTENSIVE DISORDERS IN PREGNANCY
ETIOPATHOGENESIS
• Hypertension is one of the most common medical concerns encountered in pregnancy
• Classified into four major categories:
Gestational Hypertension
° Chronic Hypertension
Chronic Hypertension with Superimposed Preeclampsia
Preeclampsia-eclampsia (preeclampsia (with or without severe features, eclampsia,
HELLP Syndrome)

I. PATHOPHYSIOLOGY
• Placental implantation with abnormal trophoblastic invasion of uterine vessels
• Immunologic maladaptive tolerance between maternal, paternal (placental), and fetal tissues
• Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy
• Genetic factors including inherited predisposing genes and epigenetic influences

II. RISK FACTORSFOR HYPERTENSIONDISORDERS IN PREGNANCY

CATEGORY
I RISK FACTOR

• Obesity (BMI ;;,30)

Maternal Factors
• Family history of preeclampsia
• Primiparity

■
Obstetric and • History of preeclampsia
gynecologic Factors • Molar pregnancy
• Multiple pregnancies
• Immunologic habituation to paternal antigens through contact
between the sperm and the female genital tract
Paternal Factors: • New sexual partner will expose the mother to new paternal
Primipaternity antigens to which she may not be tolerant
• A man who has fathered a preeclamptic pregnancy in a different
woman
• Diabetes mellitus (DM)
Medical Conditions • Anti-phospholipid syndrome (APS or APAS)
• Systemic lupus erythematosus (SLE)
• Urinary tract infection (UTI)
Infection
• Periodontal disease
Source:CPGon Hypertension in Pregnancy.POGS;2015
CunninghamFG,et.al.WilliamsObstetrics25thEdition.2018

261
III. DEFINITION OF TERMS
TERM
I CRITERIA FOR DIAGNOSIS
• Hypertension known to predate conception or detected <20 weeks
of gestation & persists at least 12 weeks post delivery
Chronic 0 Blood pressure (BP) cut off is systolic blood pressure (SBP)
Hypertension of 2140, diastolic blood pressure (DBP) of 290, or both
0 Elevated BP should have been documented in at least twice and
measurements were done at least 4 hours apart
• New-onset BP elevations (SBP 2140, DBP 290, or both)
220 weeks of gestation in the absence ofproteinuria & features of
Gestational preeclampsia
Hypertension • BP levels return to normal by 12 weeks postpartum
• Failure of BP to normalize postpartum requires changing diagnosis
to chronic hypertension
• Diagnosis in women with HPN only in early gestation who develop
proteinuria 220 weeks of gestation, or women with proteinuria
<20 weeks of gestation who develop:
Chronic 1. Sudden exacerbation of HPN or need to escalate therapy
Hypertension with 2. New-onset signs/symptoms (increase in liver enzymes, RUQ
Superimposed pain, severe headache)
Preeclampsia 3. Platelet decrease to <100,000 umol/L
4. Pulmonary edema
5. Renal insufficiency
6. Sudden and sustained increase in protein excretion
• New-onset BP elevations (SBP 2140, DBP 290, or both)
220 weeks of gestation with proteinuria (2300 mg per 24-hour
urine collection), or protein:creatinine ratio 20.3, or urine dipstick
reading 2 + 1, OR
• In the absence of proteinuria, new onset hypertension with new
onset of any of the following
Preeclampsia 0 Impaired liver function (2x elevation ofliver transaminases)
0 Persistent cerebral/visual symptoms (e.g., headache, blurring of
vision)
• Pulmonary edema
Renal insufficiency (creatinine 97 µmol/L or 1.1 mg/dL or
"'
·.;
Q,
0

doubling of creatinine in the absence of renal disease)

E 0 Thrombocytopenia (platelet count <100,000 umol/L)
u"'
.,
Cl>

·.;
• Patient with preeclampsia presenting with any of the following
0 SBP 2160, DBP 2110, or both on 2 occasions at least 4 hours
Q, apart while a patient is on bed rest
E 0 Impaired liver function (2x elevation of liver transaminases)
"'
"Q Preeclampsia 0 Persistent cerebral/visual symptoms (e.g., headache, blurring of
'" with severe
... features
'"
0..
vision)
0 Pulmonary edema
0 Renal insufficiency (creatinine 97 µmol/L or 1.1 mg/dL or
doubling of creatinine in the absence of renal disease)
0 Thrombocytopenia (platelet count <100,000 umol/L)
• Development of seizures that cannot be explained by other causes
Eclampsia in a patient with preeclampsia
• Generally considered an indication for immediate delivery of the fetus
• Unique presentation of preeclampsia (Hemolysis, Elevated Liver
HELLP
enzymes, Low f!atelets)
Syndrome
• Generally considered an indication for immediate delivery of the fetus
Source:CPGon Hypertension ,n Pregnancy.
POGS;2015
Gestational
Hypertension
& Preeclampsia: ACOGPracticeBulletin.ObstetGynecol;2020
OnaDID.et al. 2020CPGfor the Management
of Hypertension
in the Philippines.
J ClinHypertens
(Greenwich)
2021.
262
 Systolic BP • <160 mm Hg • 2'160 mm Hg
Diastolic BP • <110 mm Hg • 2'110 mm Hg
Glinical Manifestations
Gestational age • Late onset • Early onset
Headache
Visual disturbances
Upper abdominal pain
• Absent • Present
Oliguria
Convulsion (eclampsia)
Pulmonary edema
Labor:atorJ!Parameters
Serum creatinine • Normal • Elevated
Proteinuria
Thrombocytopenia
Serum transaminase
(<100,000/µL)
elevation
• None to positive

• Absent
• Mimmal
• None to positive

• Present
• Marked
I
•
SourceCunningham
FG,et al W1ll1ams
Obstetrics25thEd1t1on,
2018 :
CPGon Hypertensionin Pregnancy.
POGS;2015

B. Diagnostic Criteria for HELLPSyndrome (Two Major Definitions for HELLPSyndrome)

1. Mississippi Classification
• This system further classifies the disorder based on the platelet count any time during
the course of the disease

I CLASS 1 I CLASS 2 I CLASS 3

• 100,000-
Platelet Count • <50,000/µL • 50-100,000/µL
150,000/µL
AST or ALT • >70 IU/L • >70 IU/L • >70 lU/L
LDH • >600 IU/L • >600 IU/L • >600 IU/L
Source:MartinJN Jr.,et al. Hypertension
in Pregnancy;
2012

2. Tennessee Classification
• This system proposed strict criteria for "true/complete" HELLP syndrome when all of
the findings in the platelet count and liver enzymes are found and "partial/incomplete"
HELLP syndrome when any one of the findings are noted
COMPLETE/TRUE I INCOMPLETE/PARTIAL
• Severe preeclampsia with any one of the following:
• Platelet< 100,000 0 Elevated liver enzymes, low platelet count
• AST >70 IU/L 0 Hemolysis, elevated liver enzymes
• LDH > 600 IU/L 0 Elevated liver enzymes
0 Low platelet count
Source:CPGon Hypertension in Pregnancy.
POGS;2015
Sibai,B.Obstetricsand Gynecology;
2004
Haram,K, et al. BMCpregnancyandchildbirth;2009

263
MANIFESTATIONS AND DIAGNOSIS OF HYPERTENSIVE DISORDERS
I. MANIFESTATIONS

Elevated BP prior
• No • Yes • No
to pregnancy
• <20 weeks AOG
Onset of BP
• ;,20 weeks AOG ( even before • ;,20 weeks AOG
elevation (AOG)
pregnancy)

Proteinuria • No • May be present • Usually

Thrombocytopenia • No • No • In severe cases

High transaminases • No • No • In severe cases
Clinical Symptom
• Scintillations
Visual disturbances • None • None
• Scotomata

• Headache
• Visual
Central nervous
• None • None disturbances
system findings
• Seizure (for
eclampsia)
• Right upper
quadrant
tenderness
due to liver
Gastrointestinal inflammation
• None • None
findings • Increased
intrahepatic
pressure and
stretching of the
Glisson capsule

• May have LVH • Sudden

Cardiovascular
• None (long-standing worsening in
findings
hypertension) edema

• Arteriolar constriction
• Retinal
• Arteriovenous nicking
vasospasm
Ophthalmologic • Cotton wool spots
• None • Papilledema
findings • Yellow hard exudates
• Flame-shaped
(for longstanding
hemorrhages
hypertension)
Source: CPG on Hypertensionin Pregnancy.POGS:2015
CunninghamFG, et.al. WilliamsObstetrics25th Edition.2018

264
II. LABORATORYWORKUP AND PROCEDURES
LABORATORY I REMARKS
Ge.neral Wolik Up
Complete Blood Count • Check for presence of anemia & thrombocytopenia
• Check for presence of chamber enlargement (e.g., LVH),as
12LECG
a manifestation of chronicity
Blood Chemistry
• Sodium • Check for secondary causes of hypertension and
• Potassium comorbidities such as diabetes mellitus
• Creatinine • Check for end organ damage for chronic hypertension
• Blood urea nitrogen • Check for diagnosis of preeclampsia
• Albumin • Check for presence of features of severe preeclampsia
• Glucose level
Thyroid-stimulating
• Check for secondary causes of hypertension
hormone
• To evaluate presence of LVHamong patients with chronic
2D Echocardiography hypertension or possible structural heart disease in
patients presenting with pulmonary edema
,.,
Evalu!Jtion ofPreeclampsia-Eclampsia
• Check for diagnosis of preeclampsia
Liver enzymes {AST,ALT)
• Check for presence of features of severe preeclampsia

24 hour urine collection
Spot urine collection
Chest radiograph with
abdominal shield
Cranial CT Scan/MRI of
the brain
Abdominal Ultrasound
Electroencephalography
Fetal monitoring
■
• Determination of creatinine clearance & protein excretion
• For calculating protein/creatinine ratio
• Dipstick for detection ofproteinuria
• Evaluate presence of pulmonary edema among patients
with preeclampsia with severe features
• Evaluation for other causes of seizure such as
hemorrhage, mass or stroke
• Evaluate liver for patients with RUQpain and/or elevated
transaminases
• Evaluation of recurrent seizure activity
• Monitor fetal activity and growth (fetal well-being)

265
MANAGEMENT OF HYPERTENSIVE DISORDERS IN PREGNANCY
I. PRINCIPLESIN THE MANAGEMENTOF HYPERTENSIONIN PREGNANCY
A. Factors to Take into Consideration
FACTORS I REMARKS
• Once 34 weeks AOGis reached, delivery may be recommended for
Age of gestation
maternal and fetal safety
• HELLP and eclampsia mandates delivery, regardless of AOG
• Severe preeclampsia patients are usually delivered once 34 weeks
Severity of
AOGis achieved
disease
• Conservative measures at <34 weeks in high-risk centers
• Preeclampsia without severe features can be managed as out-patient
• Regular monitoring of multiple-organ symptoms, vital signs, body
weight, input & output, laboratory tests.
• Close monitoring of women with gestational hypertension or
Maternal
preeclampsia without severe features:
evaluation
Daily assessment of symptoms and fetal movement
0

Daily monitoring of blood pressure at home

0

Weekly assessment of platelet counts and liver enzymes

0

• In patients with gestational hypertension:

At least once weekly BP monitoring with proteinuria assessment
0
Monitoring
in the office
Additional weekly measurement of BP at home or in the office
0

• Monitor fetal movements regularly

• Fetal growth monitoring every 2-4 weeks (fetal biometry)
• Doppler studies if with evidence of fetal growth restriction
Fetal status
• NST,CST,and/or biophysical profile
• Antenatal steroids in case there is a need to deliver prematurely
• Nursery capability for 34 weeks babies

B. Conditions Precluding Expectant Management in Hypertensive Disorders in Pregnancy

0 Expectant management is NOT RECOMMENDEDin the presence of any of the following
maternal or fetal conditions:
MATERNAL CONDITION I FETAL CONDITIONS
• Uncontrolled severe BP (persistent SBP 2'160 • Abnormal fetal testing
mmHg or DBP 2'110 mm Hg not responsive to • Fetal death
medications) • Fetus without expectations for
• Persistent headaches, refractory to treatment survival at the time of maternal
• Epigastric pain or right upper quadrant pain diagnosis (e.g.. Lethal anomaly,
unresponsive to repeated analgesics extreme prematurity)
• Visual disturbances, motor deficit or altered • Persistent reversed end-diastolic
sensorium flow in the umbilical artery
• Stroke or myocardial infarction
• HELLP syndrome
• New or worsening renal dysfunction (serum
creatinine >1.1 mg/day or twice baseline)
• Pulmonary edema
• Eclampsia
• Suspected acute placental abruption or vaginal
bleeding in the absence of placenta previa
Source:GestationalHypertension
and Preeclampsia, 2020
Obstetrics& Gynecology;

266
 C. Timing of Delivery for Pregnant Patients with Hypertensive Disorders
DISORDER
I TIMING
Chronic hypertension • 38 weeks
Gestational hypertension • 37 weeks
Preeclampsia with non-severe features • 37 weeks
Preeclampsia with severe features • 34 weeks
Chronic hypertension superimposed preeclampsia • 37 weeks
Chronic hypertension superimposed preeclampsia with severe features • 34 weeks
Source:CPG on Hypertensionin Pregnancy.POGS;2015
Cunningham,FG, et al. WilliamsObstetrics25th Edition.2018

D. Indications for Delivery in Preeclampsia Regardless of AOG

MATERNAL INDICATIONS
• Eclampsia
• Recurrent symptoms of severe preeclampsia
• Uncontrollable severe hypertension
• Progressive renal insufficiency
• Persistent thrombocytopenia or HELLPsyndrome
• Pulmonary edema
• Suspected abruptio placentae
• Progressive labor or rupture of membranes
I FETAL INDICATIONS
• Severe fetal growth restriction
• Persistent oligohydramnios
• Abnormal fetal surveillance tests
(biophysical profile, umbilical artery
Doppler studies, decelerations on NST)
• Fetal death in utero

■
Source:ACOG.Task Force Recommendationon Hypertensionin Pregnancy,2013
GestationalHypertension& Preeclampsia:ACOGPracticeBulletin.Obstet Gynecol;2020

II. MANAGEMENTOF GESTATIONALAND CHRONIC HYPERTENSION

• No consensus when to initiate drug therapy
• Most guidelines recommend initiation or up titration of previous meds for women with
SBP 2'150 and/or DBP 2'100 mmHg
• First line drugs are methyldopa, calcium channel blockers or beta blockers
• ACE-inhibitors and angiotensin receptor blockers are not recommended
• Antihypertensives to maintain SBP at 130-155 mm Hg and DBP at 80-105 mm Hg

Summary of Medications Used for Hypertension in Pregnancy

DRUG
I DOSE
I REMARKS AND SIDE EFFECTS
• 500 mg to 3 g/day in
Methyldopa • Drug of choice
2 divided doses
• 200 to 1200 mg/day in
Labetalol • Fetal growth restriction
2 to 3 divided doses
• 30 to 120 mg/day ofa • Inhibits labor
Nifedipine
slow-release preparation • Synergistic action with MgSO4 in lowering BP
• SOto 300 mg/day in
Hydralazine • Neonatal thrombocytopenia
2 to 4 divided doses
• Decrease uteroplacental blood flow
Other • Depends on the • Impair fetal response to hypoxic stress
B-blockers preparation • Risk of FGRif started in 1st or 2nd trimester
• Neonatal hypoglycemia at higher doses
• Volume contraction & electrolyte disorders
Hydro-
• 12.5 to 25 mg/day • Useful in combination with methyldopa &
chlorothiazide
vasodilator to mitigate compensatory fluid retention
Source:CPG on Hypertensionin Pregnancy.POGS;2015
Reportof the NationalHighBloodPressure EducationProgramWorkingGroupon HighBloodPressure in Pregnancy.
AmericanJournalof Obstetrics& Gynecology2000; 183:S1-S22.
Ona DID,et al. 2020 CPG forthe Managementof Hypertensionin the Philippines.J ClinHypertens(Greenwich)2021.
267
III. MANAGEMENTOF ACUTESEVEREHYPERTENSION
• Defined as SBP ;;:160 and/or DBP ;;:110 mmHg persisting for ;;:15 minutes
• Start antihypertensive therapy as soon as reasonably possible (within 30-60 minutes)
after the criteria for acute onset severe hypertension are met

A. Pharmacologic Options
DRUG*
I DOSE AND ROUTE I MONITORING
• 10 to 20 mg IV,then
20 to 80 mg q20-30 mins • Adjust dose within the infusion rate
• Infusion rate: 1-2 mg/min range to achieve target BP
• Max dose: 300 mg
Labetalol
• Monitor BP at 10-minute intervals
• If BP uncontrolled after 10 mins,
• 20 mg IV over 2 minutes
give 40 mg IV over 2 minutes, and
consider referral to Cardiology
• Give 5 or 10 mg IV over
2 minutes • Monitor BP at 20-minute intervals
• ·If SBP 160 or DBP 110, • If BP uncontrolled after maximum
Hydralazine give another 5 or 10mg dose is given, give second-line
hydralazine up to a antihypertensive and consider
maximum cumulative dose referral to Cardiology
of20 mg in 24 hours
• 10 to 30 mg immediate • Given if IV access is not yet available
release capsule, every 20 • If BP uncontrolled after 50-60 mg of
Nifedipine** minutes for up to 3 doses immediate release nifedipine, give
• Immediate release capsule another antihypertensive ( usually
given per orem (not sublingual) hydralazine)
• 10 mg+ 90 cc D5W
• Infusion rate: 1 mg/hr
• Adjust dose to achieve target BP, c/o
Nicardipine** • Titrate every hour with
IM/Cardiology
increments of 1 mg/hr
• Max dose: 10 mg/hour
'Caution ifwithMgS04
.. The first-lineof treatmentis IVhydralazineand labetalol.IVnicardipineis consideredas a second-lineoption.
Extendedrelease oral nifedipinemay also be consideredas first-linetherapy,particularlywhen IVaccess is not
available.
Source:Committeeon ObstetricPractice.Obstetricsand gynecology;2015;AGOG;2015.
RobertsJM,et al. Hypertension;2003
CPG on Hypertensionin Pregnancy.POGS;2015

B. Goals in the Management of Acute Severe Hypertension

0 Goal is not to bring the BP to normal non-pregnant levels but to maintain a range of
SBP 140-150 and DBP 90-100 mmHg (to prevent repeated, prolonged exposure to
severe systolic hypertension while maintaining adequate uteroplacental perfusion)
0 Once BP is controlled, maintenance therapy (similar to chronic and gestational
hypertension) is initiated

C. Other Aspects in Management

0 When acute onset severe hypertension is diagnosed in the outpatient clinic setting,
patients are advised admission and bed rest for close maternal and fetal monitoring
° Fetal monitoring is also done to check status

268
IV. MANAGEMENTOF PREECLAMPSIA
A. Prevention of Preeclampsia
Universal Screening for Preeclampsia
• All pregnant women should be screened for between 11 weeks to 13 617 weeks using:
0 Maternal risk factors
0 Biomarkers (mean arterial pressure, uterine artery Doppler, serum placental growth factor)
• If resources are limited, routine screening for preeclampsia should include maternal risk
factors and mean arterial pressure
Women at High Risk for Preeclampsia should be given:
• Aspirin prophylaxis ("'150 mg at night) starting at 11-14 weeks gestation (or <16 weeks) until
36 weeks AOG,when preeclampsia is diagnosed
• For women with low calcium (Ca2 ') intake (<700 mg/d), give Ca'· replacement
(;el g elemental Ca'' /day) or supplementation (1.5-2 g elemental Ca''jday)
Source:PoonLCet al. International
Journalof Gynecology
& Obstetrics;2019

B. Preeclampsia with Severe Features

0 Prompt delivery irrespective of AOG in the presence of any of the following:
• Uncontrolled severe hypertension
• Pulmonary edema
• Renal failure
• Abruptio placenta
0 If there is no indication to deliver the fetus promptly, management is based on AOG
AGE OF GESTATION I MANAGEMENT
• Stabilize mother
;,,34 weeks

■
• Deliver*

• Admit to maternal ICU

• Maternal-fetal evaluation for 24 hours
• Magnesium sulfate for 24 hours for seizure prophylaxis
• Antihypertensives for BP ;e160/;e110 or MAP>125
• Sonologic monitoring:
Assess fetal size by ultrasound every 2 weeks
0

BPS + AFI at least twice weekly

0

Umbilical artery Doppler once a week

0

• Daily NST

lf33-34 weeks, consider also:

<34weeks • Steroids**
• Deliver after 48 hours of initial steroid therapy

lf23-32 6/7 weeks, consider also:

• Steroids (24-34 weeks AOG)**
• Antihypertensives if needed
• Daily evaluation of maternal-fetal condition
• Delivery if with indications
• Delivery at 32-34 weeks

If <23 weeks, consider also:

• Termination of pregnancy
'Modeof delivery:
If>34wks:vaginaldeliveryifmaternal,fetaland cervicalconditionsare favorable
0

If<32wks:CSdue to reducedsuccessininduction(cervixat <32wksis notripeenoughforinduction

0 of labor)

.. Steroidsare onlygivenwithin24-34weeksto acceleratefetallungmaturityifearlydeliveryis foreseen.Fetal

surfactantis alreadyadequate>34weeksAOGand theremaybe no added benefitwithsteroids(althoughsome
wouldstillrecommendsteroidsup to 36 6f7weeks,forthosewhodid not receivesteroidsbefore34 weeks)
0 Betamethasone12 mg/lMq24 hoursfor2 doses, or
0 Dexamethasone6 mg/lMq12 hoursfor4 doses
Source:CPGonHypertension,nPregnancy.
POGS, 2015,Hypertens,onin Pregnancy.Report
oftheTaskForce.AGOG,
2013
Norowitz,
ER.American Journal
ofObstetrics
andGynecology:2008;SibaiBM,etal.American Journal
ofObstetrics
andGynecology;
1990
OlahKS,et al.EuropeanJournal
ofObstetrics andGynecology
Reproductive
Biology;
1993
HallDR,el al.British
Journal
ofObstetrics
andGynecology:
2000
269
C. Preeclampsia without Severe Features
° For patients <37 weeks AOG,expectant management with fetal & maternal monitoring
0 Antihypertensives are given if with BP elevation d60/2'110
0 Magnesium sulfate for seizure prophylaxis is not routinely recommended for
preeclampsia without severe features

D. Magnesium Sulfate (MgSO•) for Seizure Prophylaxis

0Drug of choice for prevention of convulsions
0Administration for prevention of eclampsia is not routinely recommended for patients
with SBP <160 mmHg & DBP <100 mm Hg and no maternal symptoms

1. General Indications for Mgso.

• Prophylaxis to prevent seizures in preeclampsia with severe features & eclampsia
• Fetal neuroprotection to prevent cerebral palsy if delivered preterm (especially if
delivery is below 34 weeks)

2. Initial Magnesium Sulfate (MgSO•) Regimen (either options may be given)

Infusion ofMgso. Regimen
• Loading dose (LD) of 4-6 grams of MgSO. + 100 mL fluid given over 15-20 mins
• Begin 2 g/hour infusion as follows: incorporate 20 grams of MgSO. + 1 L D5W and
infuse at 100 ml/hour (2 g/hour) via infusion pump. The drip rate may be reduced to
1 g/hour after 24 hours. In women with impaired renal function, maintenance dose of
only 1 g/hour may be given
• Magnesium sulfate is discontinued 24 hours after delivery
• Monitor for magnesium toxicity (see discussion below)
Intermittent Intramuscular (IM) Injections
• Give 4 g of Mgso. as a 20% solution IV at a rate not to exceed 1 g/min
• Follow promptly with a 10 g of 50% MgS04 solution: one half (5 g) injected deeply
(IM) in the upper outer quadrant of each buttock through a 3-inch-Iong 20-gauge
needle (addition of 1.0 mL of 2% lidocaine minimized discomfort)
• Every 4 hours thereafter, give 5 grams of a 20% solution of MgSO. injected deeply in
the upper outer quadrant of alternate buttocks, ensuring that there are no signs of
magnesium toxicity (see discussion below)
• Magnesium sulfate is discontinued 24 hours after delivery
Sources:RoyalCollegeof Obstetricians
and Gynecologists.
RCOG;2006
AGOGTaskForceon Hypertensionin Pregnancy.Obstetrics& Gynecology;
2013
CPGon Hypertension in Pregnancy.POGS;2015
CunninghamFG,et.al.WilliamsObstetrics25thEdition;2018

3. In the Presence of Convulsions

Mgso. Infusion:
• If convulsions persist after 15 minutes, give up to 2 g/lV as a 20% solution at a rate
not to exceed 1 g/min (up to 4 grams may be given slowly in large patients)
Other Agents (if Mgso. is contraindicated or unavailable)
• Diazepam LD of 10 mg slow IV over 2 minutes (repeated if convulsions recur), then
MD of IV infusion of 40 mg diazepam + 500 mL pNSS for the first 24 hours (infusion
rate titrated based on the level of consciousness).
• Phenytoin for prevention of convulsions, which necessitates the use of diazepam to
control the convulsions

Source:AGOG;2020;
Clinicalpracticeguidelineson Hypertension
in Pregnancy.POGS;2015
CunninghamFG,et.al.WilliamsObstetrics25thEdition.2018

270
4. Monitoring for Magnesium Toxicity:

Signs of Magnesium Toxicity:

• Urine output <30 mL/hr or <100 mL for 4 hours
• Absence of patellar reflex
• Respiratory rate of <12/minute

Monitorina for Maanesium Toxicitv:

• Monitor for signs of magnesium toxicity listed above, including periodic assessment
of deep tendon reflexes (e.g., patellar)
• Some measure serum magnesium level at 4-6 hours and infusion is adjusted to
maintain therapeutic level (4-7 mEq/L or 5-9 mg/dL)
• Measure serum Mg'' levels if serum creatinine is ;;,1.0 mg/dL

Clinical Manifestations at Different Levels of Magnesium:

MANIFESTATIONS

Therapeutic range 2-3.5 4-7 5-9

Loss of patellar reflexes >3.5 >7 >9
Respiratory paralysis
Cardiac arrest
>5
>12.5
>10
>25
Source:ACOGPracticeBulletinNo.222,GestationalHypertension

Antidote for Magnesium Toxicity:

>12
>30
_
2020 ■-
and Preeclampsia,

:
• Calcium gluconate IV (10 mL of 10% solution)

271
V. MANAGEMENTOF ECLAMPSIA
• Hospitalize patient
General • Control seizures & prevent recurrence
• Control BP
• Induce labor if cervix is favorable
• CS is reserved if:
Delivery 0 Vaginal delivery does not appear easy and imminent
° Failure to progress after induction
° Fetal compromise
• Anticonvulsant therapy continued at least 24 hours after delivery
Post-Delivery
• Ensure good BP control
Sources:Quillamor,
et al. POGSCPGon Hypertension
in Pregnancy;2015
MarianoD,et al. POGSCPGon Hypertensive
Complications
of Pregnancy;2010
WHORecommendations. WHO;2011

VI. MANAGEMENT OFHELLPSYNDROME

• Follow the 12-steps to optimal management of HELLP syndrome:
0Anticipate and make the diagnosis
0Assess the maternal condition
0Assess the fetal condition: delivery sooner or later?
° Control the BP
0Prevent seizures with magnesium sulfate
0Manage fluid and electrolytes
0Exercise judicious hemotherapy (e.g., transfusion)
0Manage labor and delivery
0Optimize perinatal care
0Intensively treat the postpartum patient
0Remain alert to the development of multiple organ system failure
° Counsel about future pregnancies

AOG I MANAGEMENT
<24weeks
• Delivery be undertaken shortly after initial maternal stabilization
(non-viable)
• Delay delivery for 24-48 hours once maternal and fetal conditions are
24to 33 6/7
stable to complete course of corticosteroids for fetal benefit
2e 34weeks • Deliver promptly, soon after maternal stabilization
'Promptdeliveryis indicatedat anyAOGifthereis DIC,liverinfarctionor hemorrhage,renalfailure,pulmonary
edema,suspectedabruptioplacenta,or non-reassuring fetalstatus
'Vaginaldeliveryis desirableforwomenin laboror withrupturedmembranesand vertex-presenting fetus,regard-
less ofgestationalage
'Cesareandeliveryis suggestedforgestationsless than30 - 32 weekswithan unfavorable cervixto avoida paten-
tiallylonginduction.However, cesareandeliveryis performedforthe usualobstetricalindications
Source:Acu,ML.POGSCPGon Hypertension in Pregnancy3rd Ed;2015
in Pregnancy:Obstetrics& Gynecology;
ACOGTaskForceon Hypertension 2013
PooleJH.MCN ClinicalIssues;1997
Sibai,B.Obstetricsand Gynecology;
2004
MagannE, et al. ClinObstetricsand Gyncology;
1999

272
 SECTION THREE
HEMATOLOGIC & IMMUNOLOGIC DISORDERS

PHYSIOLOGIC ANEMIA IN PREGNANCY

I. PHYSIOLOGIC HEMATOLOGICAL CHANGES DURING PREGNANCY
• Increase in plasma volume by 40-45%
• Increase in RBC production by 30% (450 ml ofRBCs)
• Increase in coagulation factors (i.e., procoagulant state)

II. DEFINITION OF PHYSIOLOGIC ANEMIA IN PREGNANCY

• Changes above result in drop in hematocrit by 25-30% & drop in hemoglobin by 2-4 g/dL
• Hemodilution occurs for enhanced placental perfusion for better maternal-fetal gas and
nutrient exchange

AC ·t . f A I p b WHO d US CDC

TRIMESTER

1st: 0-12 weeks <110 g/L <33%

2nd: 13-28 weeks <105 g/L <32%
3rd: 29 weeks to term <110 g/L <33%
Postpartum <100 g/L <30%
Source:CPGon IronDeficiency
Anemia,November2009 ■
B. Postpartum Resolution
• Decreases immediately after delivery (possibly from increased
Plasma
aldosterone secretion)
volume
• Back to normal nonpregnant levels at 6 weeks postpartum
Physiologic
• Resolves 6 weeks postpartum
anemia

III. IRON AND FOi.ATE REQUIREMENTS DURING PREGNANCY

• Total iron requirement is ~1000 mg over the course of pregnancy
0 300 mg: for the fetus and placenta
0 500 mg: for maternal erythrocytes
Iron 0 200 mg: excreted to the urine, gut and skin
requirements • Translated into daily needs, the requirement is approximately:
0 0.8 mg iron in the 1st trimester
0 4-5 mg iron in the 2nd trimester
0 >6 mg in the 3rd trimester
• Increased demand for folate due to the increase in RBC production
Folate
• The increased folate demand is more than met by the higher daily intake
requirements
recommended for prevention of neural tube defects (400 to 800 mcg)

III. SCREENING FOR IRON REQUIREMENTS DURING PREGNANCY

Screening for • CBCduring the first prenatal visit

Anemia • Repeat CBCat week 24-28
Screening for • Ferritin levels to screen for iron deficiency
Iron Deficiency • Optional: transferrin saturation test (TSAT)

273
IRON DEFICIENCY ANEMIA (IDA) IN PREGNANCY
• Second most common cause of anemia in pregnancy (after physiologic anemia)
• Common in reproductive-age, even in nonpregnant women

I. ETIOPATHOGENESIS
• Primarily caused by expansion of plasma volume without normal expansion of
hemoglobin

A. Other Causes of Anemia:

0 High utilization of iron, but inadequate intake of iron in the diet (nutritional)
0 Inadequate iron stores
0 Expansion in blood volume starting 2nd trimester
0 Increased iron demand for maternal hemoglobin and increased fetal needs

B. Iron Status for Women During Pregnancy and the Postpartum Period
IRON
IRON
I IRON
SUFFICIENCY I DEFICIENCY
WITHOUT
DEFICIENCY

I ANEMIA I ANEMIA (IDA)

20 weeks to Hgb 110 g/L 110 g/L <110 g/L

delivery Ferritin 12 ugL <12 ugL <12 ugL

6 months Hgb 120 g/L 120 g/L <120 g/L

postpartum Ferritin 15 ugL· <15 ugL <15 ugL
Source:POGSCPGon IronDeficiencyAnemia,November2009

II. MANIFESTATIONS
A. Signs/Symptoms
0 Easy fatigability
0 Pallor
0 Shortness of breath
0 Weakness

B. Severity of Anemia by WHO

CATEGORY I SEVERITY I HEMOGLOBIN

1 Mild 95-105 g/L

2 Moderate 80-94 g/L

3 Severe 69-79 g/L

4 Very severe <69 g/L

III. DIAGNOSIS
TEST
I REMARKS

• Low hemoglobin <105 g/L

Complete blood count • Hypochromia and microcytosis
• LowMCV
• Most sensitive test
Serum ferritin levels
• Low serum ferritin levels <15 ug/L is diagnostic for IDA
Reticulocyte count • Normal to low
Serum iron levels • Low

274
IV.MANAGEMENT
A. Considerations in Management of IDA
0 Objective is to correct the deficit in hemoglobin mass & replenishment of iron stores
0 Transfusion is not necessary, unless there is hypovolemia

Prevention and Treatment of /DA

I PREVENTION OF IDA*
I TREATMENT OF !DA**
Target • All pregnant adolescent & adult • All pregnant women diagnosed
group women with IDA

Suggested • Iron: 30-60 mg elemental iron • Iron: 100-200 mg elemental iron

scheme • Folic acid: 400 ug (0.4mg) • Folic acid: 400 ug (0.4 mg)

Frequency • One supplement daily • One supplement daily

• Continued for 3 months after

• Throughout pregnancy, beginning
Duration correction of hemoglobin or until
as early as possible
6 weeks postpartum
•Proper diet and supplementationare given even if hemoglobinis normalbecause irondepletionduringpregnan-
cy is common(especiallyduring2nd trimesterwhen hemodilutionoccurs)
.. Once hemoglobinis corrected,ironsupplementationis continuedfor 3 months to replenishthe iron stores

,-
Source: POGS CPG on IronDeficiencyAnemia;2015

B. Oral Administration of Simple Iron Compounds providing 200 mg of Elemental Iron:

0
lr on supp Iemen(ts cohme inkdifferent preparations and condta)ina specific amount of ■-
e 1ementa 1iron m t e mar et, 1t comes m iron compoun s
0 Each iron compound amount has a corresponding elemental iron equivalent (below is a
guide on which preparation has the appropriate amount of elemental iron to prescribe)

Preparations of Iron Tablets

PREPARATION

Ferrous fumarate
I IRON COMPOUND
(mg per tablet)
200
I ELEMENTAL IRON
(mg per tablet)
66

Ferrous gluconate 300 36

Ferrous sulfate (7H20) 300 60

Ferrous sulfate, anhydrous 200 74

Ferrous sulfate, exsiccated 200 60

Source: POGS CPG on IronDeficiencyAnemia;2015

V.COMPLICATIONS
OF IDA
• Increased risk of infertility
• Increased risk of preterm birth, low-birth weight, and perinatal mortality
• Associated with poor maternal nutrition
• Maternal hypoxia leads to compensation: increased placental size or placental
hypertrophy to increase 02 extraction and to compensate for the low hemoglobin

275
MEGALOBLASTIC ANEMIA
I. ETIOPATHOGENESIS
• Inhibition of DNAsynthesis leads to inadequate DNAfor mitosis, which in turn leads to
unbalanced red blood cell growth
• Usually seen in women with low intake offolate-containing food (e.g., green leafy
vegetables and animal protein)
• May develop from:
0 Hyperemesis gravidarum
0 Excessive alcohol intake

II. MANIFESTATIONS
• Similar to iron deficiency anemia

III. DIAGNOSIS
• Hypersegmented neutrophils and newly formed RBCs
• Hallmark: macrocytosis (increased MCV)
• Leukothrombocytopenia
• Nucleated RBCs

IV. MANAGEMENT
A. Prevention
If with history offolic acid deficiency: folic acid 4.0 mg daily preconception and during
0

the first trimester of pregnancy

, Recommended daily allowance (RDA) for all women of child-bearing age:
folic acid 0.4 mg daily

B. Pharma co logic Treatment

, Felic acid supplementation (1 mg/day)
, Nutritious diet (e.g., yeast, liver, dark green vegetables, peanuts)
Iron
0

V. COMPLICATIONS
• Premature births
• Fetal neural tube defects
• Cleft palate

ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APAS)

• This syndrome is an autoantibody-mediated acquired thrombophilia with recurrent
thrombosis or pregnancy morbidity
• It is an immune disorder characterized by arterial or venous thrombosis and/
or pregnancy complications in the presence of persistent laboratory evidence of
antiphospholipid antibodies (aPL)

I. ETIOPATHOGENESIS
• Can be primary or secondary in the presence of systemic lupus erythematosus (SLE)
• Anti-phospholipid (aPL)-binding plasma protein antibodies places patients in a
prothrombotic state
• Infections, oxidative stress, surgery and discontinuation of anticoagulant treatment may
induce disease exacerbation by triggering induction of antibodies to PL-binding proteins

II. MANIFESTATIONS
• Manifestations represent direct and indirect expression of venous or arterial thrombosis
and/or pregnancy morbidity
• APASshould be suspected among patients with any of the following:
0 Unexplained venous or arterial thrombotic events in young patients
Pregnancy related morbidity including fetal death after 10 weeks gestation, premature
birth due to severe eclampsia or placental insufficiency
0 Unexplained thrombocytopenia or prolongation of blood coagulation parameters

276
 MANIFESTATIONS
Venous thrombosis &
related consequences
Arterial thrombosis and
related consequences
Neurologic
manifestations
Renal manifestations
Osteoarticular
manifestations
Obstetric manifestations
Fetal manifestations
I SPECIFIC EXAMPLES
• Deep vein thrombosis or pulmonary embolism
• Livedo reticularis
• Superficial thrombophlebitis
• Thrombosis in various other sites
• Stroke, transient ischemic attack, myocardial ischemia
• Leg ulcers/digital gangrene
• Retinal artery thrombosis (amaurosis fugax)
• Avascular necrosis of bone
• Multi-infarct dementia
• Migraine, epilepsy
• Chorea, cerebellar ataxia, transverse myelopathy
• Renal artery /vein thrombosis
• Fibrous intima hyperplasia
• Arthralgia
• Arthritis
• Pre-eclampsia, eclampsia
• Recurrent miscarriage
• Preterm delivery
• Fetal loss/death
• Premature birth or fetal-growth restriction

■
Hematologic
• Thrombocytopenia, autoimmune hemolytic anemia
manifestations
Source:Harrison'sPrinciplesof InternalMedicine.19thed1t1on.
2015.
CunninghamFG,et al. Williams obstetrics;2018

Ill. DIAGNOSIS:
A. Diagnostics
0 Who to screen: women with clinical criteria for APAS
, Tests include (if detected, testing should be repeated in >12 weeks):
• Anticardiolipin antibodies (aCL) lgG & IgM
• Lupus anticoagulant (LA)
• Anti-beta-2-glycoprotein-1 antibodies (P2GP1) IgG & lgM

B. Revised Sapporo APASClassification (Sydney) Criteria

, The Sapporo criteria were revised during the 11th International Congress on aPL
, Diagnosis of APASrequires at least 1 clinical criteria and 1 laboratory criteria (See Table)

CLINICAL CRITERIA LABORATORY CRITERIA

Vascular Thrombosis
• One or more clinical episodes of arterial, venous or
small vessel thrombosis, in any tissue or organ
Pregnancy Morbidity
• ;, 1 unexplained deaths of a morphologically
normal fetus at or beyond 10th week AOG,OR
• ;, 1 premature births of a morphologically normal
neonate before 34th week AOGbecause of
eclampsia or severe preeclampsia or recognized
features of placental insufficiency OR
• ;,3 unexplained consecutive spontaneous
abortions before 10th week AOG,with maternal
anatomic or hormonal abnormalities and paternal/
maternal chromosomal causes excluded
Lupus Anticoagulant (LA)
• Present in plasma, on two or more
occasions at least 12 weeks apart
Anticardiolipin Antibody (a CL)
• lgG and/or lgM isotype in serum
or plasma, present in medium
or high titer, on two or more
occasions, at least 12 weeks apart
Anti-Beta-2 Glycoprotein-1
Antibody
• IgG and/or IgM isotype in serum
or plasma, present on two or more
occasions, at least 12 weeks apart

Source:MiyakisS, et al. ThrombHaemost.2006

277
IV.MANAGEMENT
• Selection of antithrombotic therapy depends on whether the patient has APASbased on a
prior thrombosis versus an APAS-associated pregnancy morbidity
• Consider multidisciplinary team approach (e.g., immunology, cardiology, etc.)

I Pregnant or postpartum woman I

with persistent a PL positivity

Has the patient had a

thrombosisor
I thromboembolism? I
I
j I
No

Anticoagulation:
'"
Has the patient had an
APAS-definingpregnancy Antepartum: Therapeutic-dose

I morbidity? I LMWH plus low-dose ASA

I
Postpartum: Warfarin indefinitely I
No [
I '"
Antithrombotic management: Type of APS-defining
Antepartum: Low-dose ASA pregnancymorbidity?
Postpartum
After vaginaldelivery: •
~1 fetal losses at
•
?1 preterm deliveriesof a
Intermittent pneumatic
~.10 weeks AOG morphologicallynormal infant
compressionand low-dose
ASAwhile in hospital; OR before 34 weeks AOG due to

graduated compression ~3 unexplainedconsecutive severe preedampsia, eclampsia,

spontaneouspregnancy
stockingsand low-doseASA
for sixweeks losses<10 weeks AOG
After CSdelivery: I
Prophylactic-doseLMWH and
low-doseASAfor sixweeks
J I
Antithrombotic management:
Antepartum:
Prophylactic-doseLMWH
and low-doseASA
Postpartum:
Prophylactic-doseLMWH
and low-doseASA
regardlessof route of
delivery for sixweeks
or other findingsconsistentwith
placentalinsufficiency
Antithrombotic management
(most cases):
Antepartum: Low-doseASA
Postpartum:
After vaginaldelivery:
Intermittent pneumatic
compressionand low-dose
ASAwhile in hospital;
graduatedcompression
stockingsand low-dose
ASAfor sixweeks
After CSdelivery:
Prophylactic-doseLMWH
and low-doseASAfor six
weeks

'Low-doseaspirin(ASA):80-100mg

Anticoagulation•
• Low molecular weight heparins (LMWH)are generally preferred (e.g.,enoxaparin, tinzaparin)
• Dose (prophylactic versus therapeutic) depends on the indication for anticoagulation
(see algorithm above)

I PROPHYLACTIC DOSE
I THERAPEUTIC DOSE
Enoxaparin • 40 mg SC once daily • 1 mg/kg every 12 hours
Tinzaparin • 4500 units SC once daily • 175 units/kg once daily
Unfractionated
• 5,000 units every 12 hours SC • Varies per protocol
heparin (UFH)
'Anticoagulation
can generallybe resumed4-6 hoursaftervaginaldeliveryor 6-12hoursafterCS (unlesswith
significant
riskof bleeding,activebleeding,or previousneuraxialanesthesia).Directoralanticoagulants
(e.g.,
rivaroxaban)shouldnotbe used.

Source:Lockwood CJ, et al. Uptodate;2021

Berghella,V(3rdEd).Maternal-fetal
evidencebased guidelines.CRCPress;2017
BatesSM,et al.ACCPClinicalPracticeGuidelines.Chest;.2012
278
V. PREGNANCY CONSIDERATIONS
A. Anticipated Complications
MATERNAL COMPLICATIONS
• Venous and arterial thromboembolism
• Preeclampsia
• Autoimmune thrombocytopenia
• Catastrophic APAS(rare)
I FETAL COMPLICATIONS
• Early pregnancy loss and fetal death
• Fetal growth restriction
• Preterm birth
• Abruptio placenta

B. Fetal Surveillance
Early ultrasound for accurate pregnancy
0 dating
Detailed fetal anatomic scan (congenital
0 anomaly scan)
Ultrasound every 4-6 weeks for growth,
0 amniotic fluid and Doppler studies if indicated
° Fetal surveillance tests (e.g., biophysical profile) starting at 32 weeks or earlier
depending on fetal condition

C. Preparations for Delivery

0 If patient is on LMWH, shift to unfractionated heparin at 36 weeks
0 Discontinue anticoagulation 24 hours prior to planned induction of labor or Cesarean
section

D. Timing of Delivery
° Consider at 39 to 39 ,;, weeks AOGto control timing of anticoagulation discontinuation
If clinically indicated, consider delivery at early term
0

On regional anesthesia:
0

• If on UFH: may use 6-8 hours after last dose

■
• If on LMWH: may use 2'24 hours after the last dose

279
 SECTION FOUR
ENDOCRINOLOGIC DISORDERS IN PREGNANCY
GESTATIONAL DIABETES MELLITUS (GDM)
I. ETIOPATHOGENSIS
• Diabetes mellitus (OM) recognized during pregnancy should now be classified as either:
0 Gestational diabetes mellitus (GDM)
0 Overt diabetes mellitus
• Insulin resistance in pregnancy is mediated by placental section of growth hormone,
corticotropin-re!easing hormone, placental lactogen (chronic somatomammotropin),
prolactin and progesterone
• GDMoccurs when pancreas in pregnant women cannot overcome the pregnancy-induced
insulin resistance

A. Definition of Terms
TERM I DEFINITION
Pregestational
• OM diagnosed in a woman even before pregnancy
DM
• Diagnosed in the 2nd and 3rd trimester of pregnancy that is not
clearly overt OM
Gestational
• The word "gestational" implies that diabetes is induced by pregnancy
DM(GDM)
• Most important perinatal correlate is excessive fetal growth
(primary effect attributed to GDMis macrosomia)
• Pregnant woman who meets the standard non-pregnant criteria for
OvertDM
diagnosis of OM

B. Complications/Effects of Diabetes in Pregnancy•

MATERNAL COMPLICATIONS I FETAL COMPLICATIONS
• Shoulder dystocia • Spontaneous abortion
• CS delivery • Preterm delivery
• Preeclampsia • Malformations: cardiac malformations
• Infections (>50%)
• End-organ damage • Altered fetal growth: macrosomia
0 Nephropathy • Fetal demise
0 Retinopathy • Polyhydramnios
0 Neuropathy • Re~piratory distress syndrome
'Adverseconsequencesof GDMdifferfromthoseof pregestational
diabetes.Unlikein womenwithovert
diabetes,womenwithGDMdo notappearto havefetuseswithsubstantially
higherratesof anomalies
thanthe
generalpregnantpopulation

280
II. DIAGNOSIS(One-Step Strategy)
A. Screening for GDM:
0 Universal screening for GDM is recommended for Filipino gravidas
0At the first prenatal visit, determine if the gravid is high risk or not based on historical
and pregnancy risk factors

PROFILE* I SCREENING RECOMMENDATION

• All pregnant patients with any risk factors should be screened at first
High risk for prenatal visit with an FBS, HbAlc, or RBS
GDM • Those with negative screening result should be screened again at
24-28 weeks AOGusing a 2-hour 75 gram OGTT**
No risk factors • Women with no risk factors should be screened at 24-28 weeks AOG
forGDM using a 2-hour 75 gram OGTT**
FBS:fastingbloodsugar
RBS:randombloodsugar
OGTT:oralglucosetolerancetest

•Riskfactorsinclude:priorGDM,glucosuria,familyhistoryor first-degreerelativewithT2DM,PCOS,age >25

yearsold,overweight or obesity,macrosomiain previousor currentpregnancy,and polyhydramnios in current
pregnancy
.. Ifthe OGTTat 24-28weeksis normal,the womanshouldbe re-testedat 32 weeksor earlierifsigns/symptoms
of hyperglycemia are presentbothin mother& fetus(e.g.polyphagia, polyhdramnios, acceleratedfetalgrowth)

Screening for Filipino Gravidas:

■
• All Filipino gravidas are considered "high risk" by race or ethnic group (Pacific Islander)
• All should be screened for type 2 DM in the first prenatal visit (FBS, HbAlc, or RBS)
• For Filipino gravidas with no other risk factors aside from race or ethnicity and the
initial test (FBS, HbAlc or RBS) is normal, screening for GDMshould be done at 24-28
weeks using a 2-hour 75 gram OGTT.If there are other risk factors identified, screening
should proceed immediately to 2-hour 75 gram OGTTat first consult
POGSCPGon DiabetesMellitusin Pregnancy,November2011

B. Criteria used in Screening

1. Diagnosis ofGDM
• Screening should be based on the IADPSGcriteria using the 75 g OGTT (see below for
details on 75 g OGTT):

Any of the following:

• Fasting blood glucose: ;?92 mg/dL
• 1 hr OGTT:;?180 mg/dL
• 2 hr OGTT:;?153 mg/dL

2. Diagnosis of Overt DM in Pregnancy

Any of the following in their first visit•:
• Fasting blood glucose: ;?126 mg/dL (7 mmol/L)
• HbAlc ;?6.5%
• RBS ;?200 mg/dL (11.lmmol/L) + symptoms of hyperglycemia
• 2 hour 75 g OGTT;?200 mg/dL (11.1 mmol/L)
•Appliesto womenwithoutknowndiabetesantedatingpregnancy
Source:IADPSGRecommendations. DiabetesCare2010
Jimenoet al. UNITE
forDiabetesPhilippines.
2011
POGSCPGon DiabetesMellitus
in Pregnancy,November2011

281
 C. Procedure for the 75 g OGTT:
0 Ask the patient to have at least 3 days of unrestricted carbohydrate intake (>150 g
carbohydrate daily)
0 Perform the test in the morning (7-9 am) after an 8-14 hour overnight fast (water is
allowed). Smoking or physical activity are not permitted during the test.
0 Extract the initial fasting blood glucose (FBS) sample.
0 Give the patient a standard 75 g glucose solution in 250-300 mL of water, to be
ingested within 5 minutes.
0 Extract blood samples after 1 hour post-prandial glucose (PPG) and 2 hours PPG of the
glucose load
, The test should not be done during acute illness

Source:Paulweber8, et al. HormMetabRes. 2010

IV.MANAGEMENT
A. Medical Nutrition Therapy (MNT)
° Consists of an assessment of food intake, physical activity, medication history /intake,
weight management, and energy intake (during and after pregnancy)
This may be administered as a sole management approach, if sufficient to maintain
0

normal glycemic control or it may be combined with pharmacologic therapy

R d d D ·1 C 1 . I t k d ™. ht G .

PREGRAVID BMI CATEGORY I CALORIC INTAKE

(Kcal/kg/day)
I TOTAL WEIGHT GAIN
kg (lbs)
Underweight (BMI <18.5) 35-40 12.5-19 (<28-40)
Normal (B\VII18.5-24.9) 30 11.15 - 16 (25-35)
Overweight (BMI 25-29.9) 22-25 7-11.5 (15-25)
Obese 1-11(BMI >29.9) 22-25
5-9 (11-20)
Obese III (BMI >40kg/m 2) 12-14
Source:Hone,Jet al. J ClinEndocrinolMetab.2010
Dietary Recommendations
• Consumption of carbohydrates with low, instead of high, glycemic index is recommended
• Intake of sugar substitutes (e.g., acesulfame potassium, aspartame, sucralose) are
acceptable during pregnancy /lactation within acceptable daily intake limits
• General diet structure: three meals and 2-4 snacks
35-45% complex high fiber carbohydrates
0

18-20% protein of high biologic value

0

,;30% fats
0

Lifestyle Changes
• Advise against alcohol consumption and smoking
• If without contraindications, maintain sufficient level of physical activity & exercise

B. Monitoring
Women with GDM on diet treatment alone: monitor capillary blood glucose levels 4x a
0

day (fasting blood glucose once a day and postprandial blood glucose 3x a day)
Women on pharmacological therapy may monitor 4 to 6 times a day and include
0

preprandial values

Glucose Targets for Pregnant Women

GESTATIONAL DM I PREEXISTING TYPE 1 & TYPE 2 DM
• Fasting blood glucose (FBS):
,;95 mg/dL (5.3 mmol/L) • FBS 60-99 mg/dL (3.3-5.4 mmol/L)
• 1-hr Post-prandial Glucose (PPG): • PPG 100-129 mg/dL (5.4-7.1 mmol/L)
,;140 mg/dL (7.8 mmol/L) • HbAlC < 6.0 %
• 2-hr PPG ,;120 mg/dL (6.7 mmoJ/L)
Source:ADAGuidelines;2017;CPGon DiabetesMellitusin Pregnancy.POGS;2011
282
 C. Insulin Therapy
0 Optimal for women with GDMor type 2 DM who are not able to maintain
normoglycemia with a carbohydrate-restricted diet is insulin
0 Implemented if:
• Glycemic goals not met after 1 week MNT
• Fetal macrosomia or abdominal circumference> 70th percentile on ultrasound
0 May use isophane insulin (NPH), detemir, regular insulin, lispro or aspart insulin

D. Oral Hypoglycemic Agents

° For pregnant patients with overt diabetes already on metformin prior to pregnancy,
consider continuing metformin as long as glucose control is maintained (if not, may
shift to insulin therapy)

V. LABOR AND DELIVERY

A. Timing and Mode of Delivery
0 Deliver a patient with DM before 38 weeks AOGonly for compelling maternal or fetal
indications
0 DM with no complicating factors: may await spontaneous labor & allowed to progress
to expected date of delivery (as long as conditions below are met)
0 Presence of obstetric or OM-related complications (i.e.,vasculopathy, nephropathy, poor
glucose control, or prior stillbirth): elective delivery should be considered at 38 weeks

MODE I CONDITIONS

• Antenatal testing, fetal kick counts, EFMremains reassuring

• Fetus is not macrosomic (<4,000 g)
Spontaneous
• DMis well-controlled and no complicating factors
labor
• Expectant management beyond EDDgenerally is not recommended ■
a_f_te_r_c_s_de_l_iv_e_r_y_(T_O_L_A_C_J
o_f_I_a_b_o,_·
1-------+--•-D_M_is_n_ot_a_co_n_t_r_ai_n_d_ic_a_ti_o_n_t_o_t_ri_a_l -----1 : ·.·

Elective CS • Fetus is suspected to be significantly macrosomic

• EFW2:4000 grams
Source:CPGon DiabetesMellitus in Pregnancy.POGS;2018
MooreTR,et al. Diabetesmellitusand pregnancy.Medscape;2011
LamberRMJ.Guidelinesforlntrapartum Careof DiabeticWomen;2007

B. General Measures During Labor

0 Last insulin dose is given subcutaneously the night before or that morning
0 Monitor plasma glucose every 1 to 4 hours
0 Give short-acting insulin via IV infusion at a dose of 0.5-1.0 unit/hour for plasma
glucose above 120 mg/dL
0 Targets of control during labor are:
• Plasma glucose: 80-120 mg/dL (4.4-6.7 mmol/L)
• Capillary glucose: 70-110 mg/dL (3.9-6.1 mmol/L)
0 Discontinue IV insulin immediately prior to delivery

VI. POSTPARTUM MANAGEMENT

• Persistent hyperglycemiain early puerperium is uncommon & can be excluded by
measuring fasting or random capillary blood glucose levels before discharge
• Elevatedvaluesshould be confirmedwith fastingplasmaglucose(>126 mg/dL or 7.0
Post- mmol/L) or postprandial glucose (>200 mg/dL or 11.1 mmol/L)
delivery • MNT +/- pharmacologic therapy should be continued to maintain good glycemic
control & provide sufficient calories for lactation and infant well-being
• Alltypes of insulin, glyburide, or glipizide can be safely used by breastfeeding
women
• Women with a history of GDMshould:
Postpartum 0 Be screened for DMat 6-12 weeks postpartum using non-pregnant OGTT

period criteria
0 Havelifelongscreening for the development of DMat least every 3 years

Sources:MetzgerBE,et al. DiabetesCare;2007

ADAStandardsof medicalcare indiabetes.DiabetesCare;2011
CPGon DiabetesMellitusin Pregnancy.POGS;2011
283
HYPERTHYROIDISM IN PREGNANCY
I. ETIOPATHOGENESIS
• Transient increase in hCG during the first trimester, which stimulates the TSH receptor
• Estrogen-induced rise in thyroxine-binding globulin (TBG) during the first trimeste1;
which is sustained during pregnancy
• Changes in the immune system, leading to the onset, exacerbation, or amelioration of an
underlying autoimmune thyroid disease
• Complications of hyperthyroidism include:
Heart failure O Low birth weight
Thyroid storm O Spontaneous abortion
Preeclampsia O Premature labor
, Fetal death

II. MANIFESTATION
• Recall that normal pregnancy simulates some findings similar to thyroxine excess
• Suggestive findings of thyrotoxicosis include tachycardia that exceeds that usually seen
with normal pregnancy, thyromegaly, exophthalmos, and failure to gain weight

A, General Presentation of Hyperthyroidism

SIGNS I SYMPTOMS
• Hand tremor • Anxiety
• Lid lag • Increased perspiration
• Muscle weakness • Heat intolerance
• Systolichypertension with wide pulse pressure • Hyperactivity
• Tachycardia or atrial arrhythmia • Nervousness
• Warm, moist, smooth skin • Palpitations
• Weight loss despite increased appetite

B. Obstetric Manifestations of Hyperthyroidism

MANIFESTATION
I REMARKS
• Subclinical or mild overt hyperthyroidism (slightly low serum
Gestational TSH & high-normal or mildly elevated serum free T4) near the
thyrotoxicosis end of first trimester
• Normalizes between 14 to 18 weeks age of gestation
• Low TSH, with normal free T4 & T3 using trimester-specific
Subclinical
normal reference ranges or total T4 and T3 that are less than 1.5
hyperthyroidism
times the non pregnant range
• Graves' disease generally ameliorates during pregnancy
• PTU should be used during the first trimester due to the risk
Graves disease in of aplasia cutis with methimazole; PTU can be safely shifted to
pregnancy methimazole during the second trimester
• Goal FT4: Upper limit of the normal non-pregnant reference
range, using lowest dose possible
• Severe nausea and vomiting due to hCG-induced transient
Hyperemesis gestational hyperthyroidism during the first trimester
gravidarum • No treatment needed unless concomitant Graves' disease is
suspected
• Patients with molar pregnancy or gestational trophoblastic
neoplasia may present with thyrotoxicosis due to the effect of
Gestational
tumor-derived hCG upon the TSH receptor
trophoblastic
disease • Cross-stimulation only occurs at very high levels of hCG
• Treatment involves beta-blockers, anti-thyroid drugs
(controversial), and removal of underlying cause

284
III. DIAGNOSIS
• Diagnosis made based on clinical manifestations and thyroid function tests
• Confirmatory findings for hyperthyroidism:
, Markedly depressed TSH
, Elevated serum FT4 or FT3

Trimester-Specific Reference Values For Thyroid Function Tests In Pregnant Filipino Women
TEST I 1ST TRIMESTER I 2ND TRIMESTER I 3RD TRIMESTER
TSH (uIU/mL) 0.05 - 4.24 0.13 - 3.95 0.20 - 3.00
FT4 (pmol/L) 9.80 - 21.88 9.10 -18.95 9.16-18.64
FT3 (pmol/L) 2.40 - 6.20 2.77 - 5.00 2.09 - 3.70
Source:Patal,P; et al. JAFES2016

IV. MANAGEMENT
• Maintain persistent but mild hyperthyroidism to prevent maternal complications and
fetal hypothyroidism
• Pharmacologic treatment for those with moderate to severe hyperthyroidism

DRUGS I REMARKS
• Preferred treatment for overt hyperthyroidism in the first trimester
Propylthiouracil
• May be shifted to methimazole in the 2nd trimester if patient cannot
(PTU)
tolerate PTU or has an adverse response to it

■
• Started during the 2nd trimester, but associated with embryopathy if
Methimazole used in the first trimester
• Other side effects: esophageal or choanal atresia, aplasia cutis
Beta-Blockers
• Used to treat tachycardia and tremors
(Metoprolol or
• Avoid long term use in pregnancy (not more than 2 to 6 weeks)
Propranolol)

285
V. THYROID STORM
A. Etiopathogenesis
Life-threatening condition that develops in cases of untreated thyrotoxicosis
0

Precipitating factors: labor, infection, preeclampsia, severe anemia, surgery

0

B. Manifestations
° Fever, tachycardia disproportionate to fever, mental status alterations, vomiting,
diarrhea, dehydration, cardiac arrhythmias, congestive heart failure
Rarely seizures, shock, stupor and coma
0

C. Diagnosis
° Clinical testing with confirmatory testing show increased FT4 (or increased FT3) and
very lowTSH

D. Management
0 Refer to IM/Endocrinology for further evaluation and management
Therapeutic options:
0

• PTU 600-800 mg PO, then 150-200 mg PO Q4-6

• Starting 1-2 hours after PTU administration, SSKI 2-5 drops PO QB, or Lugol's
solution 8 drops Q6, or Na· iodide 0.5-1 g IV QB, or lithium carbonate 300mg PO Q6
• Dexamethasone 2mg IV or IM Q6 x 4 doses
• Propranolol 20-80 mg PO Q4-6, or 1-2 mg IV every 5 minutes for a total of 6mg,
then 1-10 mg IV Q4
Supportive therapy may include antipyretics for fever, antibiotics for infection, or heart
0

failure regimen for cardiac decompensation

E. Obstetric Management
Thyroid storm is not an absolute indication for delivery
0

Priority is to control the medical condition

0

Source:CPGon MedicalComplications in Pregnancy.POGS;2015

EckerJL, et al. CurrentProblemsin Obstetrics,Gynecology,and Fertility;2000
MolitchME.Bailliere'sClinicalEndocrinologyand Metabolism;1992

HYPOTHYROIDISM IN PREGNANCY
• Women should ideally achieve euthyroidism before conception
• Thyroid function should be evaluated immediately after pregnancy confirmation and
every 4 weeks during the first half of pregnancy, which may be decreased to every 6-8
weeks after 20 weeks' gestation

I. ETIOPATHOGENESIS
• Changes in the immune system, leading to the onset, exacerbation, or amelioration of an
underlying autoimmune thyroid disease
• Increased thyroid hormone metabolism by the placenta
• Increased urinary iodide excretion

II. MANIFESTATIONS
SIGNS I SYMPTOMS
• Bradycardia • Blurred vision
• Coarse, brittle, straw-like hair • Cold intolerance
• Coarse facial features • Constipation
• Dull facial expression • Decreased appetite
• Goiter (simple or nodular) • Decreased perspiration
• Hoarseness • Dry skin
• Hyporeflexia with delayed relaxation • Depression, emotional !ability, forgetfulness
• Macroglossia • Fatigue, lethargy, sleepiness
• Pericardia! effusion • Hair loss
• Periorbital puffiness • Inability to concentrate
• Pitting edema of lower extremities • Sleepiness
• Weight gain
286
III. DIAGNOSIS
• Diagnosis made based on clinical manifestations and thyroid function tests
• Thyroid function tests compatible with hypothyroidism:
0High TSH
0 Low FT4

IV.MANAGEMENT
• Goal TSH: <2.5 m!U/L for the first trimester and <3.0 m!U/L for the second and third
trimesters
• Separate intake oflevothyroxine from prenatal vitamins and iron supplements by at least
4 hours
• Thyroid hormone requirements are increased by up to 50% during pregnancy
• Daily iodine intake of at least 250 ug is recommended during pregnancy

A. Overt Hypothyroidism (1st trimester TSH: >10 m!U/L)

Treat ALL regardless of FT4 level
0

Begin Levothyroxine (LT4)

0

B. SubclinicaI Hypothyroidism (1st trimester TSH: 2.5-10 mIU)

FT4 LEVEL
FT4 below 5th percentile
FT4Normal
FT4 Normal, TPO negative
FT4 Normal, TPO positive
I REMARKS
• Begin levothyroxine (LT4)
• Obtain TPO
• No treatment: repeat thyroid function test in 4-8 weeks
• Begin Levothyroxine (LT4)

■
C. Monitoring of Treatment
0 Monitor TSH and FT4 every 4 weeks until 20 weeks: adjust LT4 dose to maintain
TSH <2.5 in the first trimester
0 Obtain TSH and FT4 between 26-32 weeks: adjust LT4 dose to maintain TSH <3.0 in
the 3rd trimester
0 Obtain TSH and FT4 at 6 weeks postpartum

FG,et al.WilliamsObstetrics25thEdition;2018
Source:Cunningham
CPGon MedicalComplicationsin Pregnancy.POGS;2015

V. COMPLICATIONS
SPECTRUM I COMPLICATIONS
• Maternal: gestational hypertension, preeclampsia, increased
Overt placental weight
Hypothyroidism • Fetal: cretinism, low birth weight, fetal demise, spontaneous
abortion, IUGR
• Miscarriage
Subclinical • Placental abruption
hypothyroidism • Preterm delivery
• Low IQ at age 7-9
• Spontaneous miscarriage
Complications • Recurrent miscarriage
associated with
• Preterm delivery
TPO (+)
• Placental abruption
Source:Stagnaro-Green, et al, JAMA,1990
FG,et al.WilliamsObstetrics25thEdition;2018
Cunningham
Negro,et al.J ClinEndocrinol Metab.2006

287
 SECTION FIVE
LUNG DISORDERS AND INFECTIONS IN PREGNANCY
BRONCHIAL ASTHMA IN PREGNANCY
I. ETIOPATHOGENESIS
• Hallmarks: reversible airway obstruction from bronchial smooth muscle contraction,
vascular congestion, tenacious mucus, and mucosa! edema
• Asthma is an obstructive lung disease characterized by limitation of airflow that is more
marked during expiration (obstruction is reversible)
• Decreased functional residual capacity (FRC) and increased effective shunt make the
pregnant patient more susceptible to hypoxia and hypoxemia

II. MANIFESTATION
• Expected physiologic changes - rule of 1/3:
• 1/3 of patients will worsen, 1/3 of patients will improve, 1/3 of patients will remain
controlled
• Peak of asthma exacerbation is in the 2nd trimester
• Reasons for poor control and exacerbations during pregnancy:
• Mechanical/hormonal changes
• Cessation or reduction of maintenance medications because of maternal or health
provider concerns about the potential ill effects to the fetus
Increased susceptibility to respiratory viral infection (e.g., influenza)

III. MANAGEMENT
A. General Principles
, Advantages of actively treating asthma in pregnancy markedly outweigh any potential
risks of usual controller and reliever medications
, Using medications to achieve good symptom control and prevent exacerbations is
justified even when their safety in pregnancy has not been unequivocally proven

B. Drugs for Asthma in Relation to Pregnancy

SAFETY I EXAMPLES
Drugs considered • Beta-2 agonists (preferred: albuterol) • Theophylline
safe for pregnancy • Inhaled corticosteroids (preferred: budesonide) • Cromolyn
Equivocal safety • Oral steroids
• Anticholinergics
Safety data
• Montelukast
lacking
• Zafirlukast

C. Acute Exacerbations
• Inhaled corticosteroids (JCS) prevent exacerbations of asthma during pregnancy
• Bronchoconstriction may be induced by hyperventilation during active labor, and
should be managed with a short-acting beta agonist (SABA)
• During acute exacerbation, aggressive treatment with SABA,oxygen & systemic
corticosteroids prevent fetal hypoxia

D. During Labor and Delivery

• Usual controller medications should be taken, with reliever as needed.
• Caution for neonatal hypoglycemia in mothers who received SABAwithin 48 hours
prior to delivery
• If high dose SABAwas given to the mothe1; blood glucose monitoring should be done in
the first 24 hours (particularly for preterm infants)
• To any woman given systemic corticosteroid therapy within the preceding 4 weeks,
give stress-dose corticosteroids:
• Hydrocortisone 100mg IV Q8: during labor & for 24 hours after delivery
• Oxytocin & PGE2: also for labor induction & postpartum hemorrhage
• Contraindicated in pregnancy: PGF2a (carboprost) & methylergonovine

288
IV. MONITORING
• Monthly monitoring (e.g., symptom frequency, nocturnal asthma, interference with daily
activities, exacerbations, and medication use), lung auscultation, and pulmonary function
• Spirometry should be done at baseline, with peak expiratory flow (PEF) measurement on
follow-up
• Respiratory infections should be monitored and treated promptly
• Balancing risks and benefits, refrain from stepping down !CS & long-acting
bronchodilating agent (LABA) until after delivery

V. COMPLICATIONS
MATERNAL I FETAL
• Preeclampsia • Premature birth
• Gestational hypertension • Congenital abnormalities
• Preterm labor • Fetal growth restriction
• Postpartum hemorrhage • Low birth weight
Source:PedersenS, et al. GlobalInitiativeforAsthma;2017
BusseWW,et.al.ManagingAsthmaduringPregnancy;2004
CunninghamFG,et al. Williamsobstetrics;2018

PNEUMON~INPREGNANCY
I. ETIOPATHOGENESIS
• Special consideration in pregnancy state:
0Decreased immune status

■
0 Reduced ability to expectorate
• Most common etiologic agent: Streptococcus pneumoniae
• Most common cause of influenza pneumoniae: Influenza A and B

II. MANIFESTATION
Cough followed by at least 2 symptoms:
Temp ;,38°C
0 Rigors
0

RR ;,20 breaths/min
0 ° Chills or dyspnea
HR;, 100 bpm
0 Auscultatory findings (e.g., localized crackles, rhonchi)
0

Pleuritic chest pain

0

III. DIAGNOSIS
• Chest X-ray with abdominal shield
• Arterial blood gas (ABG) especially in cases where CO2 retention is suspected
• Sputum Gram stain, culture, and sensitivity studies

IV. MANAGEMENT
ETIOLOGY I MANAGEMENT
• Require hospitalization for work up and management
• Paracetamol may be given to control fever
• Antibiotics:
Bacterial 0 Macrolide: initial monotherapy (e.g., azithromycin)
° For more severe cases: 8-lactams (co-amoxiclav) + azithromycin
° For beta-lactam allergy: may use clindamycin + azithromycin

• Supportive therapy (uncomplicated)

Viral
• Neuraminidase inhibitors shorten course of illness

V. COMPLICATIONS
• Premature rupture of membranes (most frequent)
• Low-birthweight infants
• Possible intubation & mechanical ventilation

289
URINARY TRACT INFECTION (UTI) IN PREGNANCY
I. ETIOPATHOGENESIS
UTls are the most frequent bacterial infections complicating pregnancy
• Asymptomatic bacteriuria is the most common type
• Symptomatic infection includes cystitis or pyelonephritis
• Escherichia coli strains: most common etiologic agent for UT!

II. OVERVIEWOF DIAGNOSISAND MANAGEMENT

SCREENING AND MANAGEMENT
DEFINITION
I DIAGNOSIS
Asymptomatic Bactel'iuria (ASB) in Pregnancy
I PRINCIPLES

• Persistent, actively
multiplying bacteria
within urinary tract in
asymptomatic women
• May be associated with
preterm or low-birth
infants
Acute Uncomplica{eil Cyst[tis (AUC)in Pregnancy
• Lower UT!may develop
without antecedent
bacteriuria
• Presents with dysuria,
urgency, and frequency
• Pyuria and bacteriuria
are usually found
Acute Uncomplicated Pyelonephritis (AUP) in Pregnancy
• One of the most
frequent serious medical
complications of
pregnancy
• More frequent in the
2nd trimester
• Unilateral and right-
sided in most
• May have abrupt fever/
chills & flank tenderness
• Screening is done between
9th -17th week AOG,
preferably on the 16th week
• Urine culture & sensitivity
(C/S) test for screening is
recommended
• If culture unavailable,
pyuria (>10 WBC/HPF) or
gram stain (> 2 organisms/
OIF) in 2 consecutive
midstream samples is used
• Diagnosis made by utine C/S
• In the absence of urine C/S:
• Urinalysis: significant
pyuria (>8 pus cells/mm 3
in uncentrifuged urine
or >5 pus cells/HPF in
centrifuged urine)
0 Dipstick: positive
leukocyte esterase and
nitrite test
• Pre-treatment urine culture
is needed
• Urinalysis & urine Gram
stain or C/S
• Blood culture not routinely
done, unless septic
• Treatment is indicated to
reduce risk of:
• Acute cystitis &
pyelonephritis in
pregnancy
• Low birth weight &
preterm infants
• Choice of antibiotic is based
on urine C/S
• Follow-up culture should be
done 1 week after treatment
• Monitoring is done every
trimester until delivery
• Treatment indicated to
prevent spread of infection
• Start empiric antibiotics
immediately, then adjust
using urine Gram stain or
urine C/S
• Post-treatment culture 1-2
weeks after completion
of therapy to document
eradication of bacteria
• 7-day treatment with oral
antimicrobial agent safe
for pregnancy (1 day for
fosfomycin)
"
• Consider admission if with
signs of preterm labor
• Post-treatment urine C/S
to confirm resolution of
infection
• Monitor with monthly urine
cultures until delivery

290
III. ANTIBIOTICSFOR UTI IN PREGNANCY

I ASB in Pregnancy I AUC in Pregnancy I AUPin

Pregnancy**
Oral Antibiotics (FDA Risk Category}
Cefalexin (B) 500 mg BID x 7 days 500 mg QID x ?days 500 mg QID x 14 days
Cefuroxime (B) 500 mg BID x 7days 500 mg BID x ?days 500 mg BID x 14 days
Co-Amoxiclav (B)* 625 mg BID x 7 days 625 mg BID x 7 days 625 mg BID x 14 days
Fosfomycin (B) 3 g single dose 3 g single dose
Nitrofurantoin* (B) 100 mg QID x 7 days 100 mg QID x 7days
TMP-SMX* (C) 160/800 mg BID x 7d

Cefixime (B) 200 mg BID x ?days 200 mg BID x 14 days

Parenteral Antibiotics (!for AUP]

Ceftriaxone (B) 1-2 g q24 hours
Ceftazidime (B) 2 g qS hours
Ampicillin-
1.5 g q6 hours•••
Sulbactam (B)
Warning:Beforeadministeringmedicationsin pregnantpatients,theclinicianmustbe familiarwiththesideeffects&
contraindications
of therapy(beyondthe scopeof thischapter).

• Nitrofurantoin
maybe givenduringthe 2ndtrimesteruntil32 weeks.AvoidTMP-SMX
AvoidCo-amoxiclavin the2ndtrimesterdueto the riskof necrotizing
enterocolitis
in the 1stand3rdtrimesters.
(NEC)in theneonate
.. IVtherapymaybe shiftedto oraloncepatientis 48 hoursafebrile,witha recommended
(in theabsenceof urineC/S,empirictherapyshouldbe basedon localsusceptibility
.
durationof 14days
patternsof uropathogens
-
I
primaryoptionis ceftriaxone
IV)
"' Whenurinegramstainshowsgrampositiveorganisms
Source:TaskForceon UrinaryTractInfections,
PPGG-IO
PSMID;2013-2014

291
SEXUALLY TRANSMITTED INFECTIONS IN PREGNANCY
I. VAGINITIS
MANAGEMENT
MANAGEMENT
I MATERNAL EFFECTS
I PRINCIPLES
B ac t er,a lVia9mos1s (BV)
• Options (for 7 days):
• Increased risk of other
0 Metronidazole 500 mg BID
sexually transmitted
0 Metronidazole 250 mg TIO
infection
° Clindamycin 300 mg BID
• Increased risk of
• BV is sexually associated rather than • None
PROM,preterm birth,
transmitted
intraamniotic infection
• Routine screening is not recommended
and postpartum
• Routine treatment of sex partners not
endometritis
recommended
,-- ,,,.
Trichom_gniasis n ~-

• Metronidazole 500 mg B!Dx 7 days

• Metronidazole 2 g PO in a single dose
• Low birth
(for men)
weight
• Tinidazole 2 g PO single dose
• Fever,
(alternative for men & women)
• PROM respiratory
• Retesting for T. vaginalis
• Preterm birth problems, UT!,
recommended <3 months after initial
and vaginal
treatment
discharge in the
• Partners should be treated
newborn
• Breastfeeding must be withheld up to
12-24 hours after the last dose
•· ',' ·.,
Vulvovaginal candidiasis (V,V,(;}
• Topical azole therapies applied
x 7 days are recommended (e.g.,
clotrimazole, miconazole, ticonazole)
• Oral fluconazole is contraindicated
• Not sexually transmitted • Not associated with adverse pregnancy
• Treatment of sex partners is not outcomes
recommended unless they manifest
with balanitis (erythematous areas
on glans of the penis with pruritus or
irritation)
Source:CDCSTI Guidelines;2021

292
II. MUCOPURULENT
CERVICITIS

INDICATIONS FOR I MANAGEMENT

MATERNAL
FETAL/
NEWBORN
SCREENING
I EFFECTS
I EFFECTS
Chlamydia trachomatis
• Treatment in pregnancy:
• Preterm labor
0 Azithromycin 1 g PO
with PROM
as single dose (drug of
• High risk women* • Postpartum
choice), OR
• Sexual partners endometritis
'Amoxicillin 500 mg PO • Neonatal
during the 60 days •PIO
TID x 7 days pneumonia
preceding onset of • Salpingitis
• Alternative: erythromycin • Ophthalmia
symptoms should • Fitz-Hugh-
• Fluoroquinolones & neonatorum
be evaluated and Curtis
doxycycline are avoided
treated syndrome
• Test of cure at 4 weeks
• Reiter
after completion of
syndrome
therapy is recommended
Neisseria gonorrhea

• Uncomplicated infections
in pregnancy**:
° Ceftriaxone 500 mg IM
single dose, OR
° Cefixime 400 mg PO

• High risk women*

• Presumptive
chlamydia!
therapy is given
single dose, OR
, Single dose injectable
cephalosporin
regimens, PLUS
0 Azithromycin 1 gram PO
• Septic abortion
• Preterm labor
and delivery
• Gonococcal
ophthalmia
I
• PPROM neonatorum
to women treated single dose
• Chorioamnionitis • Disseminated
for gonorrhea due • All newborns are given
• Postpartum gonococcal
to high prevalence ocular prophylaxis
infection infections
of concomitant (within 1 hour after birth):
infection , 1 % silver nitrate
solution, OR
, 1 % tetracycline
ointment/solution, OR
, 0.5% erythromycin
ointment within one
hour after birth
'High riskwomen::S25years old, priorinfection,other STDs,prostitution,new sexual partners,drug abuse
.. PLUStreatmentfor Chlamydia!infection,unless it has been excluded
Source: CDCSTI Guidelines;2021

293
lll. GENITAL ULCERS

Syphilis
MANAGEMENT
I MATERNAL
EFFECTS I FETAL/NEWBORN
EFFECTS

• Early syphilis: Benzathine penicillin-G 2.4M

U single IM dose (some recommend a 2nd
dose 1 week later)
• No proven alternatives to penicillin therapy • Fetal/neonatal effects
during pregnancy • Preterm labor • Congenital syphilis
• jarisch-Herxheimer reaction: appears • Neonatal syphilis
after penicillin, charncterized by uterine
contractions accompanied by late fetal
heart decelerations

Herpes Simplex
• Localized to eye or
• Routine screening for HSV is not
mouth
recommended
• CNS disease with
• Acyclovir 400 mg TID for 7-10 days appears
encephalitis,
to be safe for use in pregnancy (>36 weeks
lethargy, irritability,
with recurrence)
tremors, temperature
• Cesarean delivery is indicated for women
dysregulation, bulging
with active genital lesions or prodromal • Preterm labor
fontanelle
symptoms
• Disseminated disease
• Women with HSV may breastfeed, if there
with multiple major
are no active HSV breast lesions
organ involvement:
• Valacyclovir and acyclovir may be used
coagulopathy, liver
during breast feeding
dysfunction, pulmonary
• Symptomatic partners should be treated
failure, death

Chancroid
• Soft chancres:
painful,
• Azithromycin lg PO as single dose, OR
• Erythromycin 500 mg PO TID x 7 days, OR
nonindurated
genital ulcers . None
• Ceftriaxone 25 mg IM single dose • Painful
suppurative
inguinal nodes

IV. GENITAL WARTS

Condyloma acumin~tum (Human paplllomavirus 6, H.: external genital warts)
• Podofilox, podophyllin, and sinecatechins
are contraindicated in pregnancy
• lmiquimod should not be used until more
data are available • Bleeding
• Options for management include: • Increased risk for
° Cryotherapy with liquid nitrogen or CS delivery if with
• Laryngeal
cryoprobe large obstructing
0 Surgical removal either
papillomatosis
by tangential condyloma or high
scissor excision, tangential shave risk of vaginal
excision, curettage, laser, or bleeding
electrosurgery
0 Trichloroacetic acid (TCA) or
bichloroacetic acid (BCA) solution
Source: CDCST! Gu1del1nes; 2021
CunninghamFG, et al. WilliamsObstetrics25th Edition.2018.

294
NON-SEXUALLY TRANSMITTED INFECTIONS IN PREGNANCY
I. VIRALINFECTIONS
CLINICAL
MANIFESTATIONS I MANAGEMENT I MATERNAL
EFFECTS
I
FETAL/NEONATAL
EFFECTS

Varicella zoster
- IL "Sc

• Congenital varicella syndrome:

• Chickenpox
• Exposure: lg chorioretinitis, microphthalmia,
(primary infection]
given withiin cerebral cortical lesion, IUGR,
• 1- to 2-day flulike
96 hrs of limb hypoplasia, cicatricial skin
prodrome followed
exposure if • Pneumonia lesions (highest risk: first 20
by pruritic vesicular
seronegative • Hepatitis weeks of pregnancy)
lesions that crust
(susceptible) • Encephalitis • Neonatal Varicella: if maternal
after 3-7 days
• Acyclovir infection occurs 1-4 weeks
• Herpes zoster
• Vaccine not after delivery (severe if
or shingles
recommended neonate is born within 7 days
(reactivation)
of onset of maternal rash)
Influenza: A (H1N1} or B
- - -
• Influenza • Pulmonary
• Fever
vaccine involvement • Neural tube defects (in some
• Dry cough
• Oseltamivir severe in studies)
• Systemic symptoms
• Zanamivir pregnancy

Rub.eola (measles)
• Koplik spots
• Fever
• Coryza,
conjunctivitis,
cough (3 C's]
• Vaccine not
recommended
Breastfeeding
allowed
• Serum lg IM
• Pneumonia
•
•
•
•
Diarrhea
Abortion
Preterm delivery
Low birthweight
• Not teratogenic
• Neonatal infection I
Mu'!'ps
-
-
• Infection of salivary • Vaccine not
gland, gonads, recommended • Spontaneous • Not teratogenic
meninges, pancreas, • Breastfeeding abortion • Fetal infection rare
etc. allowed

Rubella (German measles)

• During first 12 weeks:
• "3-day measles"
90% chance of congenital
• Mild febrile illness
• Vaccine not infection; rare after 20 weeks
with generalized
recommended • Congenital Rubella
maculopapular • Spontaneous
• Postexposure Syndrome: cardiac septa!
rash beginning on abortion
lg defects, microcephaly,
the face, spreading
cataracts, sensorineural
to the trunk &
deafness, neonatal purpura,
extremities
radiolucent bone disease

Cytomegalovirus (CMV)(most common perinatal infection in the developed world)

• Immune-
• Symptomatic CMVInfection
compromised
(syndrome]: growth
• Most are • Symptomatic women: possible
restriction, microcephaly,
asymptomatic treatment myocarditis,
intracranial calcifications,
• Mononucleosis-like • No vaccine pneumonitis,
chorioretinitis, mental/motor
syndrome: fever, available hepatitis,
retardation, sensorineural
palpable cervical • Avoid sexual retinitis,
deficits, jaundice, hemolytic
lymph nodes transmission gastroenteritis,
anemia, thrombocytopenic
or meningo-
purpura
encephalitis

295
II. BACTERIALINFECTIONS
FETAL/
CLINICAL MATERNAL
MANIFESTATIONS

Clostridium perfringens
I MANAGEMENT
I COMPLICATIONS
I NEONATAL
EFFECTS

• Fever
• Intravascular
• Tachycardia out of
hemolysis,
proportion to the
• Penicillin G jaundice,
fever • Fetal demise
• Clindamycin hemoglobinuria,
• Uterine discharge
hypotension and
and marked
renal shutdown
leucocytosis
Clostridium tetani
• Infant tetanus:
symptoms may
or may not
be apparent
immediately
• Respiratory
after birth
• Tetanus Immunization failure and
• Trismus or lockjaw because
• Tetanus lg (Passive) convulsive
incubation
seizures
period can be
as short as
24 hours & as
long as 16-30
days
Group B Streptococcus (GBS)

• Universal rectovaginal
GBSscreening culture
at 35-3 7 weeks
• Intrapartum
prophylaxis*:
• Meningitis
0 Recommended:
• Neonatal
Penicillin G (IV) • Preterm labor
• May present with sepsis
SM U initial dose, • PROM
UT! or pneumonia • Fetal death
then 2.5-3M U q4 • Chorioamnionitis
• Respiratory
until delivery
distress
0 Alternative:
Ampicillin (IV)
2 g IV initial dose,
then 1 g IVq4 until
delivery

•1ntrapartum prophylaxis for GBS indicated in:

• PreviousinfantwithGBSdisease
• GBSbacteriunaduringcurrentpregnancy
• PositiveGBSscreeningculture
• Unknown GBSstatus(culturenotdoneor resultsunknown)
andanyofthefollowing:delivery
<37weeks,
amnioticmembranerupture;,1s hours,intrapartum
temperature
;,38°C,orintrapartum
nucleicacidamplification
tesl(NAAT)positiveforGBS

296
III. PROTOZOALINFECTIONS
FETAL/
CLINICAL MATERNAL
MANAGEMENT NEONATAL
MANIFESTATIONS
I I COMPLICATIONS
I EFFECTS
Toxoplasma gondii
• Acquired from: raw/
undercooked meat • Routine screening
• Low birthweight
infected with tissue not recommended
• Hepato-
cysts or cat feces • Spiramycin: reduce
splenomegaly
with oocysts (litter, risk of congenital
• Jaundice
soil or water) infection given • Mostly
• Anemia
• Risk of infection during acute subclinical
• Neurologic
increases with infection in early • Initial infection
disease
duration of pregnancy confers
• Micro- or
pregnancy • Pyrimethamine, immunity
hydrocephaly
• Manifestations: sulfonamides &
• Learning
feve1; headache, folinic acid: eradicate
disabilities
muscle pain, fatigue, parasites in placenta
maculopapular rash, & fetus
lymphadenopathy
-
Malaria_
• Most common • Mostly
human parasitic asymptomatic

■
• Chloroquine or
disease • For those with
hydroxychloroquine:
• From female symptoms,
treatment of
anopheline the classic
choice for sensitive
mosquito manifestations • Stillbirth
Plasmodium species
• Infected of malaria are • Preterm birth
• Chloroquine-
erythrocytes typical • Low birthweight
resistant
accumulate in • Anemia and • Miscarriage
(P. falciparum):
placenta jaundice
mefloquine,
• Flu-like symptoms: • Kidney failure,
quinine sulfate with
fever, chills, coma and death
clindamycin
headaches, myalgia, (P.falciparum
and malaise infections)
Amebiasis (Entamoeba histolytica)
• Asymptomatic
intestinal or vaginal
carrier state can
be converted to
clinically overt • Metronidazole or • 68% of fatal
disease tinidazole: drug of cases of
• Most are choice for amebic amebiasis in
• None
asymptomatic colitis & invasive females were
• Amebic dysentery: disease in pregnant associated with
fever, abdominal patients pregnancy
pain and bloody
stools
• Hepatic abscess:
worst prognosis

297
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300
 TOPATIENTS
APPROACH
INGYNECOLOGY
OVERVIEW OF THE APPROACH TO PATIENTS IN GYNECOLOGY
• Gynecology is branch of medicine that specializes in the reproductive health of females
• Any condition that affects the reproductive system, such as the cervix, uterus, ovaries,
fallopian tubes, vagina, and vulva are treated under the care of gynecologists

Examination, Screening, and Immunization for Annual Health Maintenance

Basic Examination
Well woman visit
Height, weight, • Annually
&BMI
Blood pressure • Annually • Annually
• Every 3-5 years
screening
Clinical breast
• Every 1-3 years
exam
Pelvic/speculum
• As indicated /periodically
exam*

1--0_t_h_er_E_xa_m_i_n_a_t,_·o..,n
...
s~~~---.a..,.----------.----~~~~-----1 .;_. :
• Discontinue screening
0 2:3 negative cytology
tests within the past
10 years, with the
• Every 3 years most recent Pap smear
Pap Smear (sta1t at 25 • Every 3 years within the past 3 years
years old} • After hysterectomy:
discontinue screening if
without history of CIN2+
or cervical cancer in the
past 2 0 yea rs.
• May offer starting
40 years old
• Annually after 45
Mammogram • If indicated • Annually
years old
• Start not later than
50 years old
Screening
for diabetes • If indicated • Every 3 years
mellitus
• Screen at 45 years
Screening for old
• If indicated • Every S years
dyslipidemia • If normal, repeat
every S years

Colon cancer • Fecal immunochemical test: annually

• N/A
screening** • Colonoscopy: every 10 years

303
 • If with risk factors, • Start screening at
Osteoporosis
• N/A start screening at 65 years old then
screening
50 years old every 2 years

• Influenza yearly
• Influenza yearly • Influenza yearly
• Td every 10 years
• Td every 10 years • Td every 10 years
Immunizations • TDaP once
• TDaP once • TDaP once
• Herpes zoster once
• MMR, HPV • Pneumococcal once
(>59 years)
• Annually with
nucleic acid
amplification tests
(NAAT) in sexually
Chlamydia/ active 13-24 years
• As indicated
gonorrhea old
• Annually in
women >24 years
old with increased
risk of infection
HIV • Offered routinely
•Pelvicexaminations shouldbe performed Thedecisionto perform
whenindicatedby medicalhistoryor symptoms.
a pelvicexaminationshouldbe a shareddecisionbetweenthepatientandherobstetrician-gynecologist.
at 45 yearsold
.. Startcoloncancerscreening
Source:AGOG.ObstetGynecol;2018
BaturP,et al.AmJ Med;2020
Oncologists
Societyof Gynecologic (SGOP),3rdedition,2019
of the Philippines
USPreventiveServicesTaskForce.JAMA;2018,2020,2021
AmericanFamilyPhysician. Am FamPhysician;2009
CPGon Immunization for Women;POGS,2017

304
OVERVIEW OF THE GYNECOLOGIC HISTORY
I. GENERAL IDENTIFYING INFORMATION SHOULD INCLUDE:
INFORMATION I REMARKS

Last normal
menstrual • Establishes a baseline for evaluating subsequent complaints
period (LNMP)
• Describes the total number of confirmed pregnancies, regardless of the
gestational age when the pregnancy ended
• Gravidity can be confirmed by:
Gravidity • Positive pregnancy test
• Sonogram showing gestational sac or embryo
• Embryo / fetus that was passed
• Pathology report showing trophoblastic villi
Parity • Describes pregnancies continuing 2:20 weeks gestation
Abortions • Pregnancies that are terminated before 20 weeks gestation

II. COMPONENTS OF THE GYNECOLOGICHISTORY

Chief • "How may I help you?"
complaint • Patient's description in her own words is important
Present • The circumstances when the problem started, its course and
problems progression and associated symptoms
• MIDAS:
• Menarcheal age
• Interval between cycles (shortest to longest)

■
• D.uration of each monthly cycle/number of days during which
menses occurs
Menstrual • Amount of flow
History • Symptoms (e.g., dysmenorrhea)
• LNMPand previous menstrual period (PMP)
• For postmenopausal patients:
• Age of last menses
• History of hormone replacement therapy
• Presence of postmenopausal bleeding
• Patient would be asked to list all pregnancies including abortions,
molar and ectopic pregnancies.
• For deliveries, the following should be obtained;
• Date of delivery
• Gestational age at delivery
• Type and place of delivery (e.g.,normal or operative vaginal delivery,
Previous
cesarean section)
Pregnancies
• Infant birth weight
• Any complications that may have occurred
• For all other pregnancies
• Circumstances of which they took place
• Method used (e.g.,dilatation & curettage, history of methotrexate therapy)
• Complications
Vaginal/pelvic • History of sexually transmitted infections (STls), vaginitis, and pelvic
infections inflammatory disease (PID)
• Date of last human papilloma virus (HPV) typing± Pap smear
Cervical
• Frequency of screening
cancer
• Abnormal tests and treatment
screening
• HPV vaccination status

305
 • Methods used, including length and time they have been used
Contraceptive
• Effectiveness of the method
History
• Complications and adverse reactions noted
• Age at first sexual contact
Sexual
• Number of lifetime sexual partners
History
• Sexual dysfunction (e.g., dyspareunia or anorgasmia)
• Note all surgical procedures including office procedures, with particular
Gynecologic
focus on gynecological procedures (uterine, cervical, vulva1;vaginal biopsy)
surgical
procedures Date and type of procedure, diagnoses, complications
0

Past records including operative and pathology reports

0

Past Medical • Current or past illnesses

History • Hospitalizations and past surgeries
Medications • Current medications being taken including supplements
and allergies • Allergies to medications and nature of reactions
Family
• Detailed family medical history of first- and second-degree relatives
medical
history • Congenital malformations, mental retardation, reproductive loss, etc.

• Marital or relationship status

• Gender orientation, if applicable
Social History
• Level of education and occupation
• Smoking history, alcohol usage, and illicit drug use
Avocational • Ask if patient is exercising, its type and frequency
history • Ask about hobbies that may affect health or reproductive capacity

lll. COMMONGYNECOLOGIC
COMPLAINTS
COMPLAINT
I REMARKS
• Normal discharge (clear, white, or light yellow) is composed ofmucoid
secretions with desquamated vaginal epithelium & normal bacteria
Vaginal
• Ask patient about the following
discharge
0 Onset, duration, frequency, colo1; consistency, volume, and odor of
and/or itching
the discharge
0 Onset, duration, and frequency of itching
• Vaginal bleeding most often represents uterine bleeding
• Pregnancy should be excluded in any patient of reproductive age
Abnormal
• Ask patient about amount, duration, and frequency
bleeding
• It is abnormal when bleeding is associated with a change in the normal
menstrual pattern or occurs after menopause
• Defined as failure to conceive after:
0 12 months of regular intercourse without contraception in women
Infertility <35 years old, OR
0 6 months of regular intercourse without contraception in women
;,,35 years old
• Location, timing, quality, radiation, intensity and duration of symptoms
• Factors that increase, decrease or subside pain intensity
Abdomino-
• Associated triggers, signs and symptoms
pelvic pain
• Relationship of pain to the menstrual cycle and association with other
events such as coitus or bleeding, bladder and bowel symptoms
Source:LoboRA,et al. Comprehensive 7thedition;2016
Gynecology.
CarusiDA,et al. Thegynecologic
historyand pelvicexamination.Uptodale.

306
OVERVIEW OF THE GYNECOLOGIC PHYSICAL EXAM
I. PATIENT PREPARATION
• Use hospital gown that ensures comfort and modesty
• Offer option of a chaperone
• Equipment: good light sources, gloves, speculum, water-soluble lubricant
• Patient positioning:
0 Lying supine on an office examination table with the knees flexed, and with the feet
in supporting stirrups (dorsal lithotomy position)
0 The patient's head is often elevated with a pillow, or by slightly elevating the head
of the examining table

II. BREAST EXAMINATION

• Clinical breast examination is done every 3 years for women 20-39 years old and
annually for those ;,40 years old
• Characteristics of high-quality breast exam:
Sufficient duration
0 Thorough coverage of the breast
Consistent exam pattern
0 Variable pressure with the finger pads
0 Use of index, middle and ring fingers

STEPS I REMARKS

• Breasts are visually inspected

with the patient seated
• Inspection is done in 4 views:
a. Arms at sides

■
b. Arms over head A B
1
c. Arms pressed against hips
d. Leaning forward
• Observe for skin changes,
symmetry, contours and
retraction.

C D

• Patient should be instructed

to lie supine, palpation is done
in a vertical strip pattern for 3
minutes each breast using the
index, middle, and ring fingers.
• Varying pressures (light,
medium, and deep) should be
applied in small circles for the
entire breast
2 • When palpating the lateral
aspect of the breasts, ask the
patient to roll to the opposite B
hip with hand on forehead
and shoulders against the bed
(Illustration A)
• When palpating the medial
aspect breast, ask patient
to slide her flexed elbow to
shoulder level (Illustration BJ

• During inspection and palpation: observe for symmetry, skin flattening/

3 dimpling/ erythema / edema, nipple retraction/eczema/discharge, palpable
masses, tenderness, breast fixation, tissue thickening

307
III. ABDOMEN
• Perform inspection, auscultation, percussion, and palpation
• Many gynecological tumors enlarge and occupy the abdomen; an undisclosed
pregnancy may be present as well
• Be certain that the bladder is empty
• Advise patient to inform you if she feels any discomfort during the examination

IV. EXTERNAL GENITALIA

• The dorsal lithotomy is most convenient for patient and doctor, although some prefer
the patient to be in the lateral position

• The vulva and introitus should be carefully inspected beginning with

the mons pubis for normalcy and hair distribution
• Barthol in (greater vestibular) gland openings are located at ~5 & 7
Inspection
o'clock positions, lateral & posterior to the vaginal orifice
• Skene (paraurethral) glands are not palpable in a healthy individual
• Urethra is inspected for presence of caruncle and other findings
• During palpation, the condition of the labia, clitoris, anus, and
surrounding skin should be noted
• A single finger presses on the perineum, avoiding the sensitive vestibule,
Palpation
and accustoming the patient to the examiner's touch
• Urethral meatus and vestibule are exposed. pressure from the finger will
squeeze any pus from the peri-urethral glands (pus may suggest gonorrhea)

THE PELVIC EXAMINATION

• Conducted with the patient lying supine on the examining table with her legs in
stirrups and a sheet draped across her
• A pelvic exam (including external genital evaluation, speculum exam, bi manual exam
and/or rectovaginal exam) should be done in symptomatic women

I. SPECULUM EXAMINATION
• Inspect for lesions
• Assess vaginal discharge and cervical mucus
• Usually, a light source may be required to aid visualization

A. The Speculum
A speculum is an instrument which may be made of metal or plastic; it is hinged and
0

duck-bill shaped.
It is inserted into the vaginal canal, and blades are separated in order to visualize
0

the cervix and vaginal walls.

Types of Speculum
PEDERSON SPECULUM I GRAVES SPECULUM

• Blades have a narrow design to • Wider blade

accommodate a narrower vagina • With curved sides that are advantageous
• Used in younger, virginal, or nulliparous to use in parous women
patients, as well as in elderly, menopausal
women

308
 B. Speculum Examination
0Done to visualize the vagina canal and cervix
0Most commonly utilized are the Graves and Pederson specula, with each available in
several sizes corresponding to the width and length of the blades (small, medium, large or
extra large)

• Warm the speculum (via warming device or warm water); if necessary, a water-based
lubricant may be used. Hold the speculum with the non-dominant hand
• Two fingers of the dominant hand apply downward pressure on the introitus to relax
the vagina. The speculum is inserted with the transverse diameter of the blades in the
anteroposterior position (or at a 45 degree angle) with the tips pointing downward
• Once inserted, speculum should be turned so that the transverse axis of the blades is in
the transverse axis of the vagina. Blades should be inserted to their full length
• Open the blades to adequately visualize the cervix and lock the speculum in place
• Inspect the vaginal walls for lesions or discharge. Fluid discharge should be collected for
wet mount and potential culture

■
• Inspect the cervix. Any lesion should be noted & biopsy should be performed as needed

II. BIMANUALPELVICEXAMINATION
• Allows physician to palpate the uterus and adnexa
• Only if indicated in asymptomatic, non pregnant adult women
EXAMINATION OF THE UTERUS I EXAMINATION OF THE ADNEXA
Top view

• Insert the gloved index and middle fingers of the dominant hand in the vagina and place the
non-dominant hand in the lower abdomen. Water-based lubricants may be used if needed
• Palpate the vagina, cervix, uterus, adnexa and surrounding structures by using the
abdominal hand to sweep the pelvic organs downward, while the vaginal hand is
simultaneously elevating them
• Assess for size, shape, location, consistency, mobility, and tenderness of the uterus
• Assess for adnexal masses; note their size, consistency, mobility and tenderness.
• Assess the posterior cul-de-sac and utero-sacral ligaments also for masses and nodularities

309
III. RECTOVAGINALEXAMINATION
• A rectovaginal examination allows for optimal palpation of the cul-de-sac and uterosacral
ligaments, as well as the uterus and adnexa
• Performed as indicated based on symptoms or findings from pelvic examination
• Useful if:
0 Bimanual examination has been insufficient to assess the pelvic anatomy properly
0 Suspected endometriosis or pelvic mass
Symptoms involving the rectal area

• The rectovaginal exam is performed immediately after the bimanual examination.

• With the index finger still in the vaginal canal, slowly withdraw the middle finger from the
vaginal canal and slowly insert it into the rectum.
• The examiner may also ask the patient to strain against the examiner's middle finger as
this allows the sphincter to relax and decreases patient discomfort
• Check for tenderness or masses in the rectovaginal septum, cul-de-sac, and parametria
• Assess rectum for masses
Source: LoboRA,et al. ComprehensiveGynecology.7th edition;2016
Bickley,L., et al. Bates' guide to physicalexaminationand historytaking.12thed; 2017
ACOG.Obstet Gynecol;2011

310
 SECTION TWO
PROCEDURES IN GYNECOLOGY

EXAMINATION OF THE VULVA AND VAGINA

I. VULVARDERMAL BIOPSY
• Sampling of vulvar epithelial lesions that allows for adequate histopathologic examination
• Can be either diagnostic or therapeutic:
0 Diagnostic: for histopathological examination
0 Therapeutic: when entire lesion/shave been removed for biopsy

A. Used to Diagnose the following:

, Vulvar atypias
Vulvar intraepithelial neoplasia (VlNJ/low-grade or high-grade squamous
intraepithelial lesion (LSlL/HSlL)
, Extramammary Paget disease
Squamous cell carcinoma
Bartholin gland carcinoma
Basal cell carcinoma
, Vulvar melanoma
Sexually transmitted infections (STis)

B. Instrument and Procedure

KEYES DERMAL PUNCHSET

2 mm 3 mm 4 mm 5 mm 6 mm 7 mm
0

■
0 0

• Skin and subcutaneous tissue are infiltrated with local anesthetic using a small
needle and wait 5-10 minutes for anesthesia to take effect
• Press a 3- or 4-mm Keyes punch biopsy instrument against the skin to be biopsied
and gently rotate the instrument 360' to get a nice cylindrical sample
• The small core of skin and subcutaneous tissue separated by the instrument is elevated
by small tooth tissue forceps and trimmed off the base with curved Iris scissors
• No need to suture the hole that is left but make sure to apply pressure to the biopsy
site, with the base cauterized with silver nitrate sticks

311
II. VAGINALSMEARS
• Usually done in patients complaining of vaginal discharge
• Requires three glass slides, binocular microscope, normal saline solution (NSS) and
10% potassium hydroxide (KOH)
• Three most common infections:
° Candidiasis
0 Trichomoniasis
0 Bacterial vaginosis

SMEAR I REMARKS I FINDINGS

• Lactobacilli: found in normal vaginal
flora
Normal • Addition of NSS unto a glass
• WBC cells: generally indicate vaginal
saline slide
infection
solution • Allows visualization of normal
(NSS) • Yeast cells/hyphae: indicate Candida
vaginal epithelial cells as well
Smear infection
as abnormal findings
• Trichomonads: indicate
trichomoniasis
• Addition of 10% KOH unto a
Potassium
glass slide • Presence of hyphae and spores
hydroxide
• KOH causes destruction of indicate a fungal infection (Candida
(KOH)
epidermal elements (to clearly vaginitis)
Smear
visualize the pathology)
• Classifies a causative bacteria
into one of two distinct • Gram-positive rods: Normal
groups: • Gram-negative coccobacilli: Bacterial
0 Gram positive - retain the Vaginosis
Gram stain
primary dye (crystal violet) • Budding yeast or hyphae: Candidiasis
0 Gram negative - take up the • Gram-negative intracellular
color of the counterstain diplococci: N. gonorrhea cervicitis
(safranin OJ
Whiff-Amine • Addition of 10% KOHunto a • Fishy odor or amine-like smell:
Test glass slide indicate bacterial vaginosis

312
PAP (PAPANICOLAOU) SMEAR
• Procedure to obtain cells from the cervix for cervical cytology
• Screening tool for cervical intraepithelial lesions and cervical cancer
• Goal: collect cells from the transformation zone of the cervix

I. THE NORMAL CERVIX

AREA I REMARKS
• Area where the squamous epithelium of the ectocervix meets the
Squamocolumnar columnar epithelium of the endocervix
junction (SCJ) • As one ages, the SC) migrates from the ectocervix into the
endocervical canal
• Area between the new SC) and the old SC)
Transformation/ • Contains the glandular crypts
transitional zone • Squamous metaplasia occurs in this zone: the normal columnar
epithelium is replaced by normal squamous epithelium

Area of metaplastic
squamous epithelium • The transformation zone
Area of columnar (squamocolumnar junction) is
epithelium where most cervical precancer
and/or cancer lesions occur
(due to constant wear and tear/
repair)

Old SCJ
New SCJ+---1----'---+=-·<r:_7~
Transformation
zone
• Normal columnar epithelium
is replaced by squamous
epithelium
• New squamocolumnar junction
is found near the cervical os
I:.·.• :

II. GUIDELINES FOR CERVICALCANCERSCREENING

WHO 2021 Guidelines for Screening and Treatment of Cervical Pre-Cancer Lesions for
Cervical Cancer Prevention
<30years
old, general • No screening
population
• HPV DNAdetection in a screen-and-treat approach starting at the age of
30 with regular screening every 5 to 10 years
• HPV DNAdetection in a screen, triage, and treat approach starting at the
30-50 years
age of 30 yeas with regular screening every 5 to 10 years
old
• Where HPV DNAtesting is not yet operational, WHO suggests a regular
screening interval every 3 years when using VIA or cytology as the
primary screening test
• WHO suggest screening is stopped after two consecutive negative
After SO
screening results consistent with the recommended regular screening
years old
intervals among both the general population and women living with HIV
• HPV DNA detection in a screen, triage, and treat approach starting at the
age of 25 years with regular screening every 3 to 5 years
Women
• Where HPV DNAtesting is not yet operational, WHO suggests a regular
with HIV
screening interval every 3 years when using VIA or cytology as the
primary screening test
WHO2021Guideline
forScreeningandTreatmentof CervicalPre-cancerLesionsforCervicalCancerPrevention
313
ACS 2020 Cervical Cancer Screening Recommendation
<2 5 years old • No screening
• Primary HPV test alone every 5 years (preferred)
• Use an FDA approved HPV test for primary screening
~ 25 to 65 years old
• Acceptable options: co-testing (HPV testing in combination
with cytology) every 5 years or cytology alone every 3 years
> 65 years old with
• Discontinue cervical cancer screening with any modality if
• no history of CIN grade
with adequate negative prior screening*
2 or a more severe
• Individuals aged >65 years without documentation of prior
diagnosis within the past
screening should continue until criteria for cessation are met
25 years, and
• documented adequate
negative prior screening*
in the 10 year period
before age 65 years old
• Follow age-specific screening recommendations (same as
After HPV vaccination
unvaccinated individuals)

• Individuals without a cervix and without a history of CIN 2 or

After hysterectomy a more severe diagnosis in the past ZS years or cervical cancer
ever should not be screened
'2 consecutivenegative primaryHPVtests, or
2 consecutivenegative co-tests, or
3 consecutivenegative cytologytests withinthe past 10years, withthe most recent test occurringwithingthe past
3-5years, dependingon the recommendedintervalforthe test used
Fonthamet al. CervicalCancer Screeningfor Individualsat AverageRisk:2020 Guideline
Update fromthe AmericanCancer Society.
III. REPORTING (PAP SMEAR REPORT)
• The Bethesda System (most used system for describing the Pap Test) provides the framework
for consistent interlaboratmy terminology for reporting of cervicovaginal cytology specimens
The Pap Smear Report includes
COMPONENT I REPORT

• Satisfactory
Specimen • Unsatisfactory (not ideal sample):
Adequacy • No cells on the slide
0Too much inflammation/blood that obscures the sample
• Negative for intraepithelial lesion or malignancy
General
• Epithelial cell abnormality
category
• Other malignant neoplasms

• Trichomonas vaginalis
• Fungal organisms (e.g., Candida spp)
Organisms • Shift of flora consistent with bacterial vaginosis
• Bacteria morphologically consistent with Actinomyces spp
• Cellular changes consistent with HSV

• Automated review
• Ancillary testing
• Interpretation/result (negative or diagnosis)
Others
• Organisms (e.g., Trichomonas, Candida, Actinomyces, Bacterial Vaginosis,
Herpes Simplex)
• Other findings (e.g., inflammation, atrophy, reactive inflammation with IUD)

HPVDNA • Test for specific high-risk and/or low-risk HPV types

testing• • Done in a similar way to the Pap test in terms of how sample is collected

'InfectionwithHPVis the most importantriskfactorfor developmentof cervicalcancer

314
IV. OBTAININGSAMPLESFOR CYTOLOGY
• Samples for cervical cytology and HPV testing are obtained during the speculum
examination
• Sample secretions from:
0
Ectocervix (i.e., external surface of the cervix]
0 Endocervical canal to evaluate the transformation zone (squamocolumnar
junction)
0 Sample the vaginal wall (optional)
• Two methods for sample collection and preparation include:

1. Conventional Cervical Cytology

• Cervical samples are smeared directly into a microscope slide after collection
• The ectocervix is lightly scraped by rotating the concave end of a small Ayer spatula
against the cervix so that the entire area around the cervical opening (os] is sampled
• The endocervix is sampled using a cytobrush or an endocervical brush
Drawbacks of Conventional Cytology Method:
0 Piling up of cells on top of each other
0 Inflammatory (pus) cells, increased mucus, yeast cells or bacteria may hide cervical cells
° Cells may be distorted if the sample is dried out (was not put in fixative
immediately)
° Cotton applicators do not yield optimal sample
0
Not all cell samples may be transferred in the slide

2. Liquid Based Cytology or Liquid Based Pap Testing

• Collecting device is placed into a liquid fixative solution and swirled (instead of
placing the sample on a slide)
• You only need one brush to sample both the ectocervix and endocervix
Advantages of the Newer Method:
° Cells are more evenly distributed
Minimize obscuring cells

I
0

° Cells are not dried up

Virtually all sample cells are collected
0

V. PATIENT PREPARATION
• Refrain from tampons, birth control foams, or vaginal creams 2-3 days before test
• No douching for 2-3 days before the test
• No sexual intercourse for 2 days before the test
• The best time is at least 5 days after the menstrual period stops

315
VI. SAMPLE COLLECTION
Ayer spatula

Cervical broom

c~

~!/!fl~
Detach head
and place in ~:
medium

A. Collection is done with patient in dorsal lithotomy position with the speculum inserted into
the vagina so that the cervix can be clearly seen. Sampling the ectocervix before the endocervix
will minimize bleeding [i.e., obscuring blood in the sample interferes with the interpretation)

B. Spatula is used to circumferentially scrape the ectocervix, while the cervical broom for
liquid-based cytology is inserted into the endocervix and rotated 180 degrees to obtain sample.

C. For conventional cytology, the Ayer spatula is smeared on a slide, while the brush head of the
cervical broom is detached and submerged in the liquid-based cytology medium.

316
Vil. INTERPRETATION
A. Negative for lntraepithelial Lesion or Malignancy
0 No signs of cancer or precancerous changes or other significant abnormalities were
found
0 Other findings may be unrelated to cervical cancer (e.g., infection)
0 Some cases may also show reactive cellular changes that are responses of cells to
irritation

B. Epithelial Cell Abnormalities

° Cells of the lining layer of the cervix show changes that might indicate cancer or a
precancerous condition
0 Divided into several groups for squamous cells and glandular cells

• Used when it is not possible to tell whether abnormal cells

are caused by an infection or another cause of irritation or by
Atypical
precancerous lesions
Squamous
• ASCofUndetennined Significance(ASC-US):most common abnormality
Cells (ASCs)
• ASC,cannot exclude a high grade lesion (ASC-H): must be
evaluated with colposcopy
• Low-Grade SIL (LSIL): low grade dysplasia or cervical
intraepithelial neoplasia
Squamous • High-Grade SIL (HSIL): indicates a more severe dysplasia & if
lntraepithelial unmanaged, 20% of patients with HSILwill progress to cervical cancer
Lesions (S!Ls) • All patients with HSIL should be evaluated with colposcopy and
the majority treated with excision or ablation, depending on age
,_ _________ a_n_d_co_l_p_o_s_co_p_y_a_n_d_b_i_o_p_sy_re_s_u_l_ts
_____________ ..... :_. :
Squamous Cell • The woman is likely to have an invasive squamous cell cancer
Carcinoma (remember, Pap Smear does not establish a definitive diagnosis)
(SCCA) • Further testing needs to be done to be sure of that diagnosis

2. Atypical Glandular Cells (AGC)

• Risk of underlying invasive cancer is 3-17%
• AGCcan sometimes be classified by the site of origin (e.g., endometrium, endocervix)
• The American Society of Colposcopy and Cervical Pathology (ASCCP)recommends that
all women with AGCundergo colposcopy with endocervical sampling
• Women >35 years or at risk for endometrial cancer should undergo endometrial biopsy

Source:LoboRA,et al. ComprehensiveGynecology. 7thedition;2016

ACOG.ObstetGynecol;2013
MassadLS,et al. J LowGenitTractDis;2013
ZweitigS, et al. GynecolOncol;1997
HandaVL,et al. OperativeGynecology 12thedition;2019

317
COLPOSCOPY
• Diagnostic technique involving visual inspection of the cervix and other areas of the
lower genital tract with a low power (3-lSx) binocular scope
• The surface contour, vascular pattern and staining pattern of changes seen with dilute
acetic acids and Lugo! iodine reflect the severity and extent of cervical abnormality and
help the clinician to select a location for biopsy confirmation

I. INDICATIONS
• Suspicious looking cervix
• ASC-H/HSIL/SCCA/ AGCon cytology
• Persistent low grade abnormalities on cytology
• Unsatisfactory quality on repeated cytology
• Infection with oncogenic HPV
• Acetopositivity on visual inspection with acetic acid (VIA)
• Positive on visual inspection with Lugo! iodine (Schiller Test)

II. INSTRUMENTAND PROCEDURE

THECOLPOSCOPE I PROCEDURE
• Low-power, stereoscopic, binocular field microscope • Speculum is inserted to visualize
with a powerful light source the cervix
• Used for magnified visual examination of the uterine • Position the colposcope
cervix to help in the diagnosis of cervical neoplasia • Normal saline is applied with a
sprayer or cotton balls, and excess
liquid is removed afterward
• Examine the cervix under a green
filter (colposcope)
• Identify distal & proximal borders
of transformation zone (inner
border is defined by entire 360°
circumference of the SC-junction)
• Apply 3-5% acetic acid and note
areas of acetowhitening
• Apply Lugo! iodine to cervix &
note areas of uptake and non-
uptake of the iodine
• Record all observation and results
• Areas of suspected lesions
should be biospied and sent for
histopathologic studies

Differential Diagnoses of Presence of Acetowhitening

• The application of3-5% Acetic acid dehydrates cells so that squamous cells with dense
nuclei reflect light and appear white
• Acetowhite change is noted in metaplastic cells, dysplastic cells, and cells infected with HPV

IMMATURE
CIN &
SQUAMOUS
PRECLINICAL INFLAMMATION
METAPLASIA &
EARLY INVASIVE AND HEALING
REGENERATING
CANCER
I I EPITHELIUM I
• Less pale, thin, • Distributed widely
• Dense, thick opaque
Appearance translucent (not restricted to
• Well-defined borders
• Indistinct margins the transition zone)
Disappearance of • Quickly disappears • Quickly disappears
• 2 to 4 minutes
acetowhitening within 30 seconds within 30 seconds
Source:LoboRA,et al. ComprehensiveGynecology.7th edition;2016
HandaVL,et al. OperativeGynecology12thedition;2019
318
III. PRINCIPLES
I PURPOSE
Normal • Used for moistening and
saline cleaning
solution • Helpful for evaluating blood
(NSS)
vessels and leukoplakia
• To detect & evaluate any abnormal
areas or transformation zone
• Causes swelling of epithelial
3-5% acetic tissue, columnar, & any abnormal
acid squamous epithelial areas
• Causes reversible coagulation
or precipitation of the nuclear
proteins and cytokeratins
• Iodine solution confers a
Lugol's mahogany brown or nearly black
iodine squamous cells which contain
stores of glycogen
• Applied to the light source to increase the contrast of the red blood vessels
Green filter
and help clarify any vascular changes
• Suspected areas of cervical lesions should be sent for histopathologic studies
Cervical
• Can be undertaken using special instruments such as the Tischler,
biopsy
Kevorkian, Younge, or Gaylord biopsy forceps
319
I FINDINGS
• Transformation zone (light pink):
smooth translucent epithelium with a
pinkish tinge after application of NSS
• Original squamous epithelium
(more pink): No vascular patterns
are often seen
• Columnar epithelium (dark red):
with a sea anemone tentacle-like
villous appearance
• Normal squamous epithelium: little
coagulation occurs in the superficial
layers
• Areas ofCIN undergo maximal
coagulation due to their higher
content of nuclear protein (in
contrast to the normal squamous
epithelium)
• High glycogen: normal squamous
epithelium
• No glycogen: normal columnar
epithelium
• Little or no glycogen: suspicious
squamous epithelium
0 Immature squamous metaplasia
I
0 Regenerating epithelium
0 Inflammatory and congenital
transformation zone
° Condyloma
0 Abnormal transition zones (CIN or
invasive cancer)
ENDOMET~ALSAMPLING
• Endometrial sampling allows for histologic evaluation of endometrium (see indications)
either through an office endometrial biopsy or through an endometrial curettage

I. INDICATIONS AND CONTRAINDICATIONS

A. Indications:
0 Abnormal uterine bleeding (AUB-M,see Chapter 16, Section 3): endometrial
hyperplasia or malignancy
0 Postmenopausal bleeding
0 Premenopausal bleeding with risk factors for endometrial cancer
0 Presence of atypical glandular endometrial cells on cervical cytology
0 Evaluation for endometrial neoplasia or precancerous hyperplasia
0 Surveillance of previously diagnosed endometrial hyperplasia
0 Evaluation of uterine response to hormone therapy

B. Contraindications
ABSOLUTE I RELATIVE
• Pregnancy • Cervical stenosis
• Acute pelvic inflammatory disease • Clotting disorder or coagulopathy
• Acute cervical infection
• Acute vaginal infection
• Cervical cancer

II. ENDOMETRIAL BIOPSY

• Office diagnostic procedure without anesthesia but oral analgesic may be given
INSTRUMENT I REMARKS I IMAGE

Cervical • Use to grasp the anterior lip of

Tena cu I um the cervix to straighten it

• Hollow, rigid curette with a blunt

rounded tip of varying sizes
Endometrial
• Tip also features sharp,
Curette
staggered, teeth-like serrations
• Used with a suction device

• Disposable, pliable plastic

Pipelle
catheter that can be placed
Endometrial
through the cervix into the
Suction
Curette endometrial cavity for aspiration
of endometrial cells

320
lll. ENDOMETRIAL CURETTAGE
• Both diagnostic and therapeutic in cases of abnormal uterine bleeding
• Dilatation of the cervix and endometrial curettage

A. Indications
THERAPEUTIC INDICATIONS I DIAGNOSTIC INDICATIONS
• Therapeutic abortion* • Endometrial hyperplasia or cancer
• Late postpartum hemorrhage • Infertility
• Retained placental tissues
• Abnormal uterine bleeding
•mega!in the localsetting

B. Procedure
INSTRUMENTS I PROCEDURE
• Vaginal retractor
• Tenaculum forceps
• Hysterometer
• Hegar dilators
• Ovum forceps
• Uterine curettes
• Place patient in lithotomy position under anesthesia
• Aseptic technique
• Empty bladder via straight catheterization
• Sterile draping of the perineum
• Bimanual exam to evaluate uterine size and position
• Adequately expose the cervix with open-sided or weighted
speculum
• Assess the depth of uterine cavity using a hysterometer
• Dilatate cervix using Hegar dilators
• Curettage of anterior, lateral, and posterior uterine walls
using an appropriately sized curette

■
• Reassess the depth of the uterine cavity using a hysterometer

C. Complications
0 Acute hemorrhage
0 Trauma to the uterus and adjacent structures
° Cervical laceration

321
OTHER COMMON PROCEDURES IN GYNECOLOGY
• Gynecologic procedures are varied and some are done as office procedures while others are
done in the operating room
• Diagnostic procedures: colposcopy, transvaginal ultrasound, hysterosalpingography, saline
infusion sonography
• Therapeutic procedures: oophorocystectomy, salpingectomy for ectopic pregnancy, salpingo-
oophorectomy, hysterectomy

• A procedure in which a colored dye is passed through

Chromopertubation the fallopian tubes to confirm patency intraoperatively,
either via laparotomy or laparoscopy
• Surgical excision of a cone-shaped portion of the cervix
using the scalpel of laser knife, along with the entire
Cold knife conization
transformation zone
(CKC)
• Used to diagnose and treat cervical dysplasia or very
early cervical cancer
• Diagnostic procedure using a low-power binocular
microscope with a powerful light source (colposcope)
Colposcopy to carefully examine the cervix and vagina
• Visual examination of the surface lining of the lower
genital tract to identify lesions and to define its borders
• Radiographic diagnostic study of the uterus and
Hysterosalpingogram (HSG) fallopian tubes, most commonly used in the evaluation
of infertility
• Sono logic observation of the uterine architecture,
Hysterosonosalpingography
endometrial lining and cavity, as well as tubal patency,
(HSSG)
using contrast medium (usually saline solution)
• Also called a large loop excision of the transformation
zone (LLETZ)
Loop electrosurgical • Excision biopsy of the cervix performed with a thin
excision procedure (LEEP) wire electrosurgical loop electrode 1 to 2.5 cm, usually
under local anesthesia
• Both diagnostic and therapeutic
• Ultrasonic observation of the uterine architecture,
Saline infusion sonography endometrial lining and cavity interfaces following the
instillation of saline into the endometrial cavity
Transvaginal • Ultrasound imaging of the female pelvis using an
ultrasonography (TVS) endoscopic probe placed in the vagina
Access
• Surgical incision in the vagina
Colpotomy • Incision into and through the vaginal epithelium into a
cavity (often abscess or pelvic/abdominal cavity)
• Direct visual inspection of the cervical canal and uterine
Hysteroscopy
cavity through a rigid or flexible hysteroscope
• Procedure that permits visual examination of the
Laparoscopy abdominopelvic cavity with an optical instrument
(laparoscope)
• Open surgery of the abdomen to examine the
Exploratory Laparotomy
abdominal and pelvic organs, tissues and vessels

322
 PROCEDURE I REMARKS
Ther,apeutic
-
• Use of refrigerant gas (carbon dioxide or nitrous oxide)
to ablate abnormal lesions
Cryotherapy
• Tissue is cooled to -20°C to cause crystallization of
intracellular water and destroy the lesion
• Also known as thermal cautery
• Direct or alternating current is passed through a wire
Electrocautery
electrode to generate heat
• Applied in living tissue to achieve hemostasis
• A form of coagulation attained by arcing or spraying of
"sparks" to tissue surface using high voltage, damped, or
interrupted function with active electrode not touching
Fulguration
tissue
• This is used to coagulate bleeding vessel or for treatment
of endometriosis
• Surgical removal of the uterus (total hysterectomy)
• Supracervical hysterectomy (or subtotal hysterectomy);
Hysterectomy removal of the uterine fundus, transecting the upper
portion of the cervix below the level of the uterine
vessels (cervix is left in situ)
• Surgical removal of an ovary
• Prophylactic oophorectomy: surgical removal of clinically
Oophorectomy
normal ovaries at the time of hysterectomy to reduce risk
of ovarian and, possibly, breast cancer

Oophorocystectomy
• Surgical removal of an ovarian cyst without removing the
ovaries
• Reapproximation of perinea! connective tissue including
I
Perineorrhaphy the bulbocavernosus and transverse perinea! muscles to
restore the perinea! body
Salpingectomy • Surgical removal of a fallopian tube
Salpingooophorectomy • Surgical removal of the ipsilateral oviduct and ovary
• Operative opening made in the oviduct that is used to
Salpingotomy remove an unruptured tubal pregnancy then the tube is
closed by primary intention
• Operative opening made in the oviduct that is used to
remove an unruptured tubal pregnancy then the tube is
allowed to close by secondary intention
Salpingostomy
• Can also refer to salpingoneostomy; creation of a new
stoma in an oviduct with a completely occluded distal
end such as in cases of hydrosalpinx

323
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Z.ACOG Committee Opinion No. 755: Well-Woman Visit. Obstet Gynecol. 2018 Oct;132(4):e181-e186. doi: 10.1097 /
AOG.0000000000002897. PMID: 30247364
3.ACOGPractice Bulletin - Clinical Management Guidelines for Obstetrician-Gynecologists: No. 140: Management of Abnom1a\
Cervical Cancer ScreeningTest Results and Cervical Cancer Precursors. Committee on Practice Bulletin. Obstet Gynecol.
2013;122(6):1338-136 7.
4.American College of Obstetricians-Gynecologists (ACOG).Practice bulletin no.122: Breast cancer screening. Obstet Gynecol.
2011;118(2 Pt 1):372-382.
S.American Family Physician. U.S.Preventive Se1vices Task Force screening for lipid disorders in adults: recommendation
Statement. Am Fam Physician. 2009 Dec 1;80(11):1273-1274.
6.Batur P,Phipps M, Qaseem A The Women's Preventive Services Initiative Well-Woman Chart: A Helpful Tool for the Practice
of Internal Medicine. Am J Med. 2020 Oct;133(10):1122-1125. doi: 10.1016/j.amjmed.2020.05.011. Epub 2020 Jun 18.
PMID: 32565259.
7.Bickley, L, Szilagyi, P.and Hoffman, R., 2017. Bates' guide to physical examination and history taking. 12th ed. Philadelphia:
Wolters Kluwer
8.Carusi DA,et al. The gynecologic history and pelvic examination. Uptodate.
9.Clinical Practice Guideline on Immunization for Women (2017). Philippine Obstetrics and Gynecologic Society
10. Colposcopy and treannent of cervical intraepithelial neoplasia: a beginners' manual, Edited by J.W. Sellars and R.
Sankaranarayanan Chapter 6: Colposcopic appearance of the normal cervix (https://screening.iarc.fr /colpo.php)
11. Handa, Victoria L.;Van Le, Linda (2019) Te Lindes Operative Gynecology 12th edition Lippincott Williams & Wilkins
12. Handa, Victoria L; Van Le, Linda (2019) Te Lindes Operative Gynecology 12th edition Lippincott Williams & Wilkins
13. Lefevre ML; U.S. Preventive Services Task Force. Screening for Chlamydia and gonorrhea: U.S. Preventive Services Task
Force recommendation statement. Ann Intern Med. 2014 Dec 16;161(12):902-10. doi: 10.7326/M14-1981. PMID:
25243785.
14. Lobo RA, Gershenson DM, Lentz GM,Valea FA Comprehensive gynecology. 7th edition. Elsevier, 2016
15. Massad LS, Einstein MH, Huh WK. et al. 2012 updated consensus guidelinesfor the management of abnormal cervical
cancer screening tests and cancerprecursors. J Low Genit Tract Dis. 2013;17(5 Suppl 1):Sl-S27.
16. Practice Bulletin No. 179 Summary: Breast Cancer Risk Assessment and Screening in Average-Risk Women. Obstet
Gynecol. 2017 Jul;130(1):241-243. doi: 10.1097 /AOG.0000000000002151. PMID: 28644328.
17. Society of Gynecologic Oncologists of the Philippines (SGOP) Clinical Practice Guidelines for the Obstetrician-Gynecologist.
3rd Ed.; July 2019.
18. US Preventive Setvices Task Force, Curry SJ, Krist AH, Owens DK. Barry MJ,Caughey AB, Davidson KW,Doubeni CA.Epling
JW Jr, Kemper AR, Kubik M, Landefeld CS, Mangione CM, Phipps MG,Pignone M, Silverstein M,Simon MA,Tseng CW,Wong
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K, Doubeni CA, Epling JW Jr, Kubik M, Landefeld S, Ogedegbe G, Pbe1t L, Silverstein M, Simon MA, Tseng CW. Wong JB.
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20. US Preventive Services Task Force, Owens DK. Davidson Kw, Krist AH, Barry MJ,Cabana M, Caughey AB, Curry SJ, Doubeni
CA. EplingJW Jr, Kubik M, Landefeld CS,Mangione CM, Pbert L, Silverstein M, Simon MA,Tseng CW,Wong JB. Screening for
HIV Infection: US Preventive Se,vices Task Force Recommendation Statement. JAMA.2019 Jun 18;321(23):2326-2336.
doi: 10.1001/jama.2019.6587. PMID: 31184701.
21. US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation
Statement. JAMA.2021;325(19):1965-1977. doi:10.1001/jama.2021.6238
22. Zweitig S, Noller K. Reale F,et al. Neoplasia associated with atypical glandularcells of undetermined significance on cervical
cytology. Gynecol Oncol.1997;65:314-318.

324
BENIGN DISEASES
GYNECOLOGIC
 SECTION ONE
BENIGN DISEASES OF THE VULVA AND VAGINA

DERMATOLOGIC DISEASES
• Broad spectrum of atrophic and hypertrophic conditions characterized by skin changes
due to variety of etiologic agents
• Pruritus (single most common gynecologic problem): intense itching with an associated
desire to scratch and rub the affected area

MANIFESTATIONS &
ETIOPATHOGENESIS MANAGEMENT
DIAGNOSIS
Liche!.'Simplex <thronicus
- .

• Reactive changes to • Vulvar pruritus • Topical steroids, calcineurin

chronic scratching • Thickened white epithelium
("itch-scratch cycle") with slight scaling
or rubbing (rather • Excoriation and fissures are
than hyperkeratotic common
changes) • Most commonly involves
the hair-bearing skin of the
labia majora, mons pubis,
and perianal region
• May be confined to a focal
area, appearing gray-white
or reddened
• Usually bilateral, symmetric
and can extend beyond the
labia majora
,, C·
'LichenSclerosus(LS)
• Unknown etiology
usually seen among
postmenopausal
women and
• Pruritus & vulvar discomfort
• White atrophic papules that
can coalesce into porcelain-
white papules
prepubertal girls • Lesions are always limited
• Associated with by the labia majora (if
hypoestrogenism lesions go beyond the labia
• Histologically, there is majora, the condition is
thinning of the vu Ivar unlikely to be LS)
epithelium with loss of • Extension into perineum
the rete pegs and anus: form "figure-
• Higher risk of eight" or "hour-glass" shape;
vulvar malignancy may be lichenified with a
in postmenopausal hypopigmented parchment-
women like appearance
inhibitors
• Avoidance of scratching
• Elimination of provocative
stimuli, use of lubricants,
cool sitz bath
• Medium potency topical
steroids
• Avoid irritation or trauma to
the genital epithelium, clean
labia by soaking in sitz baths
• Postmenopausal women:
I
do biopsy to rule out vu Ivar
intraepithelial neoplasia
(VIN) and subsequent
squamous cell carcinoma
• High-potency topical
corticosteroid (e.g.
clobetasol)
• Estrogen cream: for
menopausal atrophy, labial
fusion and dysparenia
• Severe cases (e.g., introital
stenosis): surgery followed
by vaginal dilation and
coritcosteroids

327
 MANIFESTATIONS &
ETIOPATHOGENESIS

Contact Dermatitis'·
I DIAGNOSIS
I MANAGEMENT

• Maybe irritant type • Acute contact dermatitis: • Elimination of offending

(immediate irritation) red, edematous, inflamed agent, restoration of
or allergic type skin; may become weeping protective skin barrier,
( delayed onset of and eczematoid reduction of inflammation,
irritation • Chronic untreated contact scratch cessation
, Primary irritant dermatitis: can evolve into a • Topical steroids
(non-immunologic): syndrome of lichenification, • Use of a barrier product
manifestations with the skin developing a such as zinc oxide ointment
disappear within leathery appearance and • Use cotton undergarments
12 hours of texture (i.e., lichen simplex and avoid tight-fitting
discontinuing the chronicus) clothing
offending substance • Vulvar skin inflammation
, Allergic origin
(immunologic):
cell-mediated
delayed-type (type
IV) hypersensitivity
reaction which
requires 36-48
hours to manifest &
persists several days
despite removal of
the allergen
..
lntertrigo u
• From friction between • Initial erythematous • Drying agents ( e.g,
moist skin surfaces appearance that can lead to anti-fungal power/zinc
usually in labiocrural erosions, exudates, fissures, oxide paste), mild topical
folds maceration and crusting corticosteroids
• Burning, itching, • Weight loss for obese
hyperpigmented changes patients
may be seen
Atopic Dermatitis II
• Most present before • Dryness & scaling • Topical corticosteroids,
age 5 and majority • Thickening of skin with emollients
of cases remit by localized excoriation if • If without response: topical
adolescence vulva has been irritated by calcineurin inhibitors
• Chronic relapsing scratching • In rare, severe cases:
course that may • Severe pruritic eruption systemic treatment with
be associated with • Scaly patches with fissures calcineurin inhibitors
development of allergic ( cyclosporine)
rhinitis and asthma • Moisturizers for dry skin
Source:KumarR, et al. Blaustein'sPathologyof the FemaleGenitalTract;2019
Lobo,et al. ComprehensiveGynecology.7th ed. 2017

328
BENIGN CYSTS & TUMORS
• Occlusion ofpilosebaceous ducts, sebaceous ducts and apocrine sweat glands
• Treatment is only needed if lesions become symptomatic or infected

ETIOPATHOGENESIS
I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Epidermal Inclusion Cysts (EiC)
• Most common small • Multiple cysts, • Simple examination • If infected: local
vulvar cyst majority <l cm in • Biopsy in some heat application,
• Skin invagination with diameter cases incision and
keratinized epithelial • Asymptomatic • Transperineal drainage
lining, stratified unless secondarily ultrasound • For recurrent
squamous epithelium infected infection or
with a center of cellular pain: excision
debris that grossly when acute
resembles sebaceous inflammation
material. has subsided
• Most epidermal cysts
do not have sebaceous
cells or sebaceous
material
Sebaceous, Cyst
- - -
• Most common tumor • Often multiple and • Biopsy • Incision &
of the vulva (together asymptomatic • Transperineal drainage
with EiC) • Sebum accumulates ultrasound
• Due to occlusion of within the cyst
sebaceous duct • May become super-
infected with local
flora
Apocrine Sweat Glarfd Cyst t

• Fox-Fordyce disease:
microcystic disease
• Hidradenitis
suppurativa: multiple
infected abscesses
• Pruritic and foul
smelling
• Biopsy
• Transperineal
ultrasound
• Wide local
excision
• Incision &
drainage
• Overlying
I
• Due to occlusion of cellulitis:
apocrine gland ducts antibiotics
in the mans pubis and
labia majora
Paraurethral Gland Cyst
• Skene duct cyst • Maybe • Biopsy • Incision &
• Due to chronic superinfected • Transperineal drainage
inflammation of ultrasound
the gland causing
obstruction of the duct
GattnerDuctCyst •s
• Dysontogenic cyst • Usually • Biopsy • Excision
• Remnants of asymptomatic • Transperineal • IYP& cystoscopy
mesonephric ducts of • Tense palpable ultrasound performed
the Wolffian system cyst that may bulge preoperatively
• Submucosal along below vaginal wall • Yasopressin
anterior or lateral wall • May present during perioperatively
of the upper vagina adolescence with
dyspareunia
or difficulty in
inserting tampons
329
ETIOPATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Bartholin Duct e.r,st and Abscess
• Due to obstruction of • Usually • Transperineal • No treatment
Bartholin gland (for asymptomatic ultrasound for 1-2 cm &
cyst) or polymicrobial • Unilateral, round, • Biopsy if indicated asymptomatic
infection or STDs (for fluctuant/tense (2:40 years old) • Sitz bath: for
abscess) usually in the pain relief &
• Bartholin gland: inner aspect of reduced healing
located entrance of the inferior labia time
the vagina at 5 & 7 majora or lower • Marsupialization:
o'clock position vestibule entire cyst
• Most common large • Pressure or abscess is
cyst of the vulva symptoms, local incised & edges
pain, dyspareunia, are sutured to
difficulty in vaginal mucosa
walking • Excision biopsy
• May be associated (2:40 years old)
with cellulitis • Word catheter
• Antibiotics
Urethral Carunclel: _ ~
- -
• Outgrowth of distal • Majority are • Biopsy (caruncle • Avoidance of
edge of urethra asymptomatic is com posed of irritation
• Due to chronic • Often secondarily transitional and • Estrogen (oral
irritation or infection infected, producing stratified squamous or topical)
• Mostly seen in ulceration & epithelium with a • Cryosurgery,
prepubertal and bleeding loose connective fulguration,
postmenopausal • Point tenderness tissue. Often the excision
women after contact with submucosal layer
• Associated with undergarments or contains relatively
hypoestrogenism during intercourse. large dilated veins)
• Ulcerative lesions • Voiding
usually produce cystourethrography
spotting on contact • Cystourethroscopy
Urethral Diverticul-qm
• Permanent • 3 D's of • Voiding • Excision if
epithelialized sac-like diverticulum: cystourethrography symptoms are
projection 0 Dysuria • Cystourethroscopy persistent or
, Dyspareunia with recurrent
0 Dribbling infection
Nevus II
• Commonly referred to • Benign nevus: • Excisional biopsy: should be adequate
as a "mole" flat, elevated, in width and depth, with ~5-10 mm of
• Localized nest sharp borders, normal skin surrounding the nevus and
or cluster of even color, and underlying dermis included
melanocytes symmetrical
• One of the most • Dysplastic: 6-20
common benign mm with diffuse
neoplasms in females margins, speckling
of color, and
asymmetrical

330
ETIOPATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Hemangioma -
• Rare malformations • Mostly • Biopsy • Resection or
of blood vessels rather asymptomatic excisional
than true neoplasms • Usually single, biopsy
1-2 cm in diameter, • Cryosurgery or
flat, and soft, and argon laser
they range in color
from brown to red
or purple
Fibroma
-
-
• Most common benign • Smaller fibromas • Biopsy • Operative
solid tumor of the are asymptomatic • Transperineal removal if
vulva • Pressure symptoms ultrasound symptomatic,
• Low-grade potential • Acute pain during grows larger,
for becoming degeneration and for
malignant • Smooth surface cosmetic
and a distinct reasons
contour
• Most commonly
found in the labia
majora
Lipoma
• Second most frequent • Asymptomatic • Biopsy • Excision for
type of benign vulvar (unless extremely • Transperineal large tumors
mesenchymal tumor large) ultrasound
• Slow-growing, • CT scan
circumscribed • MRI

■
tumors of fat cells
arising from the
subcutaneous tissue
of the vulva
Source:Lobo,et al. Comprehensive
Gynecology.
7thed. 2017

331
 BENIGN DISEASES OF THE CERVIX, UTERUS,
AND FALLOPIAN Tl'.JBES

DISEASES OF THE CERVIX

ETIOPATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT

Cervical PolJtp II .. .,, "·
'
• Most common benign • Ulceration of • Transvaginal • Polypectomy
neoplastic growth of the stalk's most ultrasound with
cervix dependent portion • Biopsy if indicated endocervical
• Most common in causes bleeding curettage
multiparous • Endocervical
• Secondary to polyps: cherry red
inflammation or • Cervical polyps:
abnormal focal grayish white
responsiveness to • Post-coital
hormones bleeding
• Adenomatous type
in80%
Nabothian_ Cyst II -
• Retention mucus • Asymptomatic • Inspection and • No treatment
cysts of endocervical • Translucent or palpation necessary
columnar cells usually opaque, whitish or • Transvaginal
at the transformation yellow ultrasound
zone • Vary from
microscopic to
macroscopic size
,~
·Cervical LeiomyoJ/.a ~- -
• Smooth, firm, solitary • Most are small and • Inspection and • Observation:
masses mostly arising asymptomatic palpation asymptomatic
from the uterine • Expanding • Transvaginal &small
isthmus myomas produce ultrasound ± • Surgery:
symptoms from Dopplers occurrence &
mechanical • Biopsy if indicated persistence of
pressure on symptoms
adjacent organs
Cervicaistenosi~ Iii '••
' ~

• Often occurs in the • Symptoms differ • Inability to • Cervical

internal os depending on the introduce a dilation under
• Maybe congenital or menopausal status cervical dilator ultrasound
acquired of the woman into uterine cavity guidance
• Transvaginal • Laminaria tent
ultrasound or T-tube as
stent for a few
days
Source:Lobo,et al. Comprehensive
Gynecology.
7thed.2017

332
ENDOMETRIAL POLYP
I. ETIOPATHOGENESIS
• Localized overgrowths of the endometrial glands and stroma projecting beyond the
endometrial surface
• Has three histological components:
, Endometrial glands
0Endometrial stroma
Central vascular channels

II. MANIFESTATIONS& DIAGNOSIS

• Mostly are asymptomatic
• Common manifestation is abnormal uterine bleeding
• Polyps are soft, pliable, and may be single or multiple
• Most are detected by sonography

III. MANAGEMENT
• Removal by hysteroscopy via transcervical resection of the polyp (TCRP)

LEIOMYOMA (MYOMA)
I. ETIOPATHOGENESIS
• Benign tumors of smooth muscle cell origin
• The most frequent pelvic tumor and the most common tumor in women
Highest prevalence at the 5th decade of woman's life
• Found in 30-50% of perimenopausal women

A. Risks Factors:
, Increasing age
, Early menarche
Low parity
0

, Tamoxifen use
, Obesity

,..B_.
0

_T...._ ■
_:_:g_:_f_f:~t._:_i:_t_a..,_b_as_e_d_o_n_l_o_ca_t_io_n-',_r_.e._e_r_to_C_h_a._t_e_r_l_6.,_or_th_e_F_I_G_O_S'-u-b_c_la-'s_s1._
,_·c_at_i_on......__~

Pedunculated '-.. Subserous

Submucous

• Intramural: located within the uterine wall.

• Subserous: protrudes into the pelvic cavity
• Submucous: protrudes into the uterine cavity.
• Other types: intraligamentary, parasitic myoma
333
 C. Degeneration
0 With continued growth, myomas outgrow their blood supply and degeneration of the
myoma occurs

TYPE OF
DEGENERATION
I REMARKS

• Mildest form of degeneration characterized by loss of smooth

Hyaline (65%)
muscle cells that are replaced by fibrous connective tissue
• Occurs in 5-10% of pregnant women
Carneous or red • Can cause severe pain and peritoneal irritation
• Characterized by extensive coagulative necrosis
• Due to the deposition of calcium phosphates and carbonates
Calcific brought about by the continued diminished blood supply and
ischemic necrosis of tissue
Cystic or • Characterized by accumulation of edema fluid and often
hydropic associated with collagen deposition
• Result from adipose metaplasia in myomas
Fatty
• Contains an admixture of smooth muscle & mature adipose tissue
• May be a misnomer
Malignant • It is unknown whether myomas degenerate into leiomyosarcomas
or whether they arise spontaneously

II. MANIFESTATIONS
• Usually asymptomatic but may include bleeding, pressure symptoms, pain, and infertility
• Symptomatic leiomyomas are the primary indication for approximately 30% of all
hysterectomies
• Pelvic examination: uterine size, as assessed by bimanual examination, correlates well
with uterine size and weight at pathologic examination, even in most obese women

III. DIAGNOSIS

DIAGNOSTICS
I REMARKS
• Typically used to confirm the diagnosis of myomas
• Complementary transabdominal ultrasound evaluation may be of
value in selected cases such as large volume myomas
TransvaginaI • Sonohysterography or saline infusion sonography (SIS)
Ultrasound (TVS) • Color Doppler with SIS: may be useful in distinguishing polyp
from submucosal myomas based on the vascularity of the lesions
0 Polyps: a single feeding vessel
0 Myoma: several vessels
Hystero-
• Mandatory in the evaluation of infertility
salpingography
• Diagnostic hysteroscopy & SIS are equivalent diagnostic tools for
Hysteroscopy
the detection of submucous myomas and polyps
• MRI is more accurate for exact myoma mapping and should be
preferred when such mapping is important
• Recommended for preoperative evaluation when extensive
MRI
surgery is planned especially for those who want to preserve
fertility
• MRI is superior to TVS for ruling out adenomyosis

334
IV. MANAGEMENT
• Myomas that are asymptomatic may be managed expectantly regardless of size & location
• Treatment is aimed at symptom reduction and/or preservation of fertility
• Medical therapy is usually targeted to symptoms of heavy menstrual bleeding
• Surgery is best for submucous myoma presenting with heavy menstrual bleeding, and
myomas causing bulk symptoms, pain, and infertility

A. Medical Management

I RATIONALE/MECHANISM I ADVERSE EFFECTS

• Induces a pseudomenopausal state
with decrease in gonadotropin levels
• GnRH agonists decreases the heavy
• Hot flashes,, sweating,
menstrual bleeding and shrinks
and vaginal dryness
myomas
GnRH agonist • Trabecular bone loss
• Decrease in size is transient, and
when used for longer
after treatment, myomas have been
than 6 months
shown to rapidly grow in size
• Usually given pre-operatively before
hysterectomy or myomectomy
• Downregulates angiogenic growth
factors - vascular endothelial
growth factors (VEGF)and causes
suppression of neovascularization • Headache, stomach
Ulipristal
and myoma proliferation pain, nausea, dizziness,
acetate*
• Induces apoptosis by increased irregular periods, fatigue
caspase-3-expression, decreased
bcl-2 expression, decreased collagen
in extracellular matrix
• Localized progesterone effect that
causes rapid decidualisation of the

■
Levonorgestrel endometrial stroma and acts on the
releasing • Irregular bleeding and
uterine vasculature and the receptors
intrauterine spotting, cramping
in myometrium that results in
system • Hepatotoxicity
(LNG-IUS) decrease in bleeding
• Some studies have shown decrease
in myomas volume with LNG-lUS
• Blocks the peripheral conve'rsion
• Hot flushes, vaginal
Aromatase of androgens to estrogen in the
dryness, musculoskeletal
inhibitors ovaries and peripheral tissues, thus
pain
decreasing estrogen
•AsofSeptember2020,the EuropeanMedicines Agency'sRiskAssessmentCommittee has recommendedthe
revocationof PharmacovigilanceMarketing Authorityforthe 5 mgoraltabletsofulipristal
acetate(UPA)generics
after5 cases ofsevereliverinjuryneedinglivertransplantwerereported
Source:ReesV,et al. EMAsafetycommittee.
EuropeanPharmaceutical
Review;2020
DonnezJ, DolmansMM.Uterinefibroidmanagement.
HumReprodUpdate;2016

335
 B. Surgical Management

I DESCRIPTION
I REMARKS

• Removal ofmyoma • Hysteroscopic myomectomy: first line

with uterine for the management of symptomatic
conservation submucous myomas
Myomectomy • Done via • Abdominal myomectomy: for myomas
hysteroscopy, 2'5-8 cm, multiple or when deep intramural
laparoscopy, or myomas are present (maybe done
laparotomy laparoscopically or through a laparotomy)

• Offered to symptomatic patients who do not

respond to medical management and are no
• Definitive surgery
longer desirous of fertility
• Involves complete
Hysterectomy • Also offered to patients with concomitant
removal of the
disease such as adenomyosis, cervical
uterus
dysplasia or uterine prolapse, for which
hysterectomy is curative for these conditions

C. Others

I DESCRIPTION
• Minimally invasive option for
management of myoma related
symptoms
Uterine artery
• Percutaneous angiographic
embolization
procedure performed with
(UAE)
video fluoroscopic imaging
with injection of embolic agents
into the uterine artery
High intensity
• Utilizes high intensity
frequency
ultrasound energy to induce
ultrasound
(HiFU) coagulative necrosis of myomas
I REMARKS
• Ideal for those with heavy
menstrual bleeding or
dysmenorrhea caused by
intramural myoma, who are
premenopausal, and who have
no desire for future pregnancy,
and who are poor surgical risk
patients
• Ideal for patients who would
want to retain their uterus,
with myomas <10cm in
maximal dimension

PARATUBAL CYSTS
I. ETIOPATHOGENESIS
• Para tubal cysts may be of mesonephric, mesothelial, or paramesonephtic orgin
• When paratubal cysts are pedunculated and near the fimbrial end of the fallopian tube,
they are called hydatid cysts of Morgagni

II. MANIFESTATIONS
• Asymptomatic (majority)
Symptoms
• When para tubal cysts are symptomatic, they usually present with dull pain
• Large and rapidly growing cysts may present with abnormal enlargement
• On physical examination, it is difficult to differentiate a paratubal cyst
Signs
from ovarian cysts
• If present, they may present as movable adnexal masses

III. DIAGNOSIS
• On transvaginal ultrasound, they are visualized as adnexal masses which are separate
from the ovaries

IV. MANAGEMENT
• If asymptomatic, expectant management is recommended
• In pregnancy, they may grow rapidly and cause torsion; in these cases, treatment is
simple excision
336
ENDOMETRIOSIS
• Presence and growth of the glands and stroma from the endometrial lining of the uterus
in an aberrant or heterotopic location
• The classic symptom of endometriosis is cyclic pelvic pain

I. ETIOPATHOGENESIS
A. Theories in Etiology
• Implantation of endometrial cells shed during menstruation
Retrograde
gaining access to the peritoneal cavity through the fallopian tubes,
menstruation
growing as homologous grafts under hormonal influence
• Endometriosis is transplanted via lymphatic & vascular system
Lymphatic • Best explains endometrial implants found in remote sites.
and vascular Hematogenous dissemination of endometrium is the best theory
dissemination to explain endometriosis of the forearm and thigh, as well as
multiple lesions in the lung
• Endometriosis arises from metapiasia of the coeiomic epithelium
Metaplasia
or proliferation of the embryonic rests
• Endometrial glands and stroma are implanted during surgical
Iatrogenic
procedure (e.g., endometriosis on abdominal incision site)
Genetic • Incidence of endometriosis in relatives of women with the disease:
predisposition 7x increase
• Those who develop endometriosis have more peritoneal
Immunologic macrophages that are larger
changes • These hyperactive cells secrete multiple growth factors and
cytokines that enhance the development of endometriosis

B. Location oflmplants in the Pelvis

Bladder----~

Iliac
vessels I
section

Cardinal
ligament

Uterus

Fallopian
tube
Round
ligament

Pelvic
peritoneum
'Blackshapesindicate
Ovary implants
endometrial
• Majority are located in the dependent portions of the female pelvis
• Ovaries (most common): ovarian endometrioma are called "chocolate cysts" due
to accumulation of old blood
• Pelvic peritoneum over the uterus and fallopian tube
• Anterior and posterior cul-de-sac
• Uterosacrai, round, and broad ligaments
• Rectovaginai septum
• Rectosigmoid

337
II. MANIFESTATIONS
• Classic symptoms: cyclic pelvic pain and infertility
• Common symptoms: pelvic heaviness, dyspareunia
• Abnormal bleeding
Symptoms
• GI and urinary tract symptoms: cyclic abdominal pain, intermittent
constipation, diarrhea, dyschezia, urinary frequency, dysuria, hematuria
• Rare: Catamenial hemothorax (thoracic endometriosis) and as cites
• Classic pelvic finding: Fixed retroverted uterus, with scarring and
tenderness posterior to the uterus
• Tenderness of the pelvic structures, nodularity of the uterosacral
ligaments and cul-de-sac
Signs
• Advanced cases: extensive scarring and narrowing of the posterior
vaginal fornix
• Ovaries may be enlarged and tender and are often fixed to the broad
ligament or lateral pelvic sidewall
'

III. DIAGNOSIS
• Pathognomonic symptoms: pelvic pain, dysmenorrhea, dyschezia, dyspareunia, and
infertility can often pinpoint to a diagnosis of pelvic endometriosis (supported by
findings of a retroverted uterus, adnexal masses, and nodularities in the cul de sac)
• Experts are advocating non-invasive means of diagnosing endometriosis
• Other diagnostic modalities: transvaginal ultrasound, MRI,and laparoscopy

DIAGNOSTICS I REMARKS
• Characteristic ultrasound findings: a unilocular cyst with homogenous
low level echogenicity
• Presence of soft markers such as absence of sliding sign may also be
Transvaginal
noted (involves using gentle probe pressure to assess whether the
or transrectaI
ultrasound
anterior rectum & sigmoid colon glide freely across the posterior
aspect of the upper uterus, cervix, and vaginal wall)
• May be able to visualize endometriotic nodules on the rectosigmoid
and uterosacral ligaments
I
• May be used in the diagnosis of deep infiltrating endometriosis
MRI
• Limited value in diagnosing superficial endometriosis
• Gold standard for diagnosis: allows for tissue biopsy which shows
endometrial glands, stroma, and hemosiderin laden macrophages
Laparoscopy • Allows for an accurate visual diagnosis and staging of disease
• Invasive procedure and should not be a prerequisite to starting
medical therapy (can treat empirically, especially for young patients)

338
IV. MANAGEMENT
• Short term goals: relief of pain and address infertility
• Long term goal: prevent progression or recurrence

A. Medical Management (primary goal: induction of amenorrhea)

CONDITION I DEFINITION
I MANAGEMENT
I
SIDE
EFFECTS
• State of androgen excess • Anti-estrogen, • Acne, weight
Pseudo- that sends negative hyperandrogenic gain, hot
virilized feedback to the brain effect (danazol* 400 flashes,
state and disrupts ovulation & to 800 mg/day for 6 deepening of
induces amenorrhea months) voice
• Hormonal state • Hot flahes,
where in there is no • GnRH agonist vaginal
Pseudo- production of estrogen (leupro!ide 3.75mg IM dryness,
menopause & progesterone from per month or insomnia&
state ovaries due to absence 11.25 mg IM for decrease in
of gonadotropins as an 3 months) mineral bone
effect of GnRH agonists density
• Monophasic combined • May cause
• The constant hormonal
OCP (1 pill daily for at irregular
levels supplied by
Pseudo- least 6 months) bleeding
OCPs or progesterone-
pregnancy • Progesterone-only • May cause
only therapy disrupts
state contraceptives (DMPA bloating,
ovulation & induces
150mg IM every 3 headaches,
amenorrhea
months) nausea
'Has fallenoutof favordue to severityof sideeffects

B. Surgical Management
0
Indications ■
erapy d
• AFailedmedical thf1 .:
• cute rupture o arge en ometriomas
• Deep infiltrating endometriosis (ureteral obstruction, compromised large bowel
function]
• Endometriotic cysts of >3 cm associated with pain & non-responsive to medications
• Endometriotic cysts of>4 cm if for assisted reproductive procedure
• Adnexal enlargements of more than >8 cm
• Patient no longer desirous of future pregnancies

Approaches to Surgical Management

• Fulguration or resection of endometrial implants
• Removal of all macroscopic, visible areas of endometriosis with
Conservative
preservation of ovarian function (oophorocystectomy) and restoration
of pelvic anatomy (lysis of adhesions J
• TAH+BSOand removal of all visible endometriosis
Definitive • Reserved for advanced disease and for whom future fertility is not a
consideration and/or perimenopausal
Combination
of medical • Postoperative medical therapy is considered depending on the
& surgical extensiveness of the disease and the success of surgery
therapy

339
ADENOMYOSIS
I. ETIOPATHOGENESIS
• Derived from aberrant glands of the basalis layer of the endometrium (compared to
endometrosis which is derived from the functionalis layer)
• Associated with aromatase expression and higher levels of tissue estrogen
• Break down between the endometrium and myometrium
• Standard histologic criterion: Presence of endometrial glands and stroma more than one
low-powered field (2.5 mm) from the basal is layer of the endometrium
PRESENTATION I HISTOPATHOLOGY
Symmetrical
• Diffuse involvement of the anterior and posterior walls of the uterus
(diffuse
adenomyosis)
resulting in a uniformly enlarged uterus (most common)

Asymmetrical
• Focal areas of adenomyotic lesions resulting in an asymmetric or an
(focal
adenomyosis)
irregular shaped uterus (often referred to as adenomyoma)

II. MANIFESTATIONS
• Asymptomatic (majority)
• Classic symptoms: dysmenorrhea & heavy menstrual bleeding
• Pain may be due to bleeding & swelling of endometrial islands
Symptoms
confined in myometrium
• Heavy menstrual bleeding is related to the increased endometrial
surface of the enlarged uterus
• Classic findings in the uterus on pelvic exam
0 Diffusely enlarged usually 2 to 3x normal size
Signs
0 Globular
, Mobile

III. DIAGNOSIS
DIAGNOSTICS I REMARKS
• A transvaginal ultrasound is the first line imaging modality
• Ultrasound findings:
0 Asymmetrical thickening of the myometrium (with the
Transvaginal posterior myometrium typically thicker)
Ultrasound 0 Presence of myometrial cysts
0 Linear striations radiating out from the endometrium
0 Loss of clear endomyometrial border
0 Increased myometrial heterogeneity
• Reserved for cases wherein it is important to distinguish diffuse and
focal adenomyosis from leiomyomas
MRI
• Allows for a quantification of the thickening of the junctional zone,
I with > 12 mm generally considered diagnostic of adenomyosis
Source:ReinholdC, et al. Radiographies;
1999

IV. MANAGEMENT
• No satisfactory medical management (e.g., GnRH agonist, cyclic hormones, prostaglandin
synthetase)
• Definitive treatment: hysterectomy

340
ENDOMETRIOSIS VERSUS ADENOMYOSIS
• Endometriosis and adenomyosis are clinically different diseases
• The only common feature is the presence of ectopic endometrial glands and stroma

I ENDOMETRIOSIS
I ADENOMYOSIS
• Presence & growth of the glands
and stroma of the endometrial
Definition
lining of the uterus in an • Endometrial glands and stroma
aberrant or heterotopic location more than one low-powered field
• Endometrial glands (2.5 mm) from the basalis layer of
• Endometrial stroma the endometrium
Histology
• Hemosiderin-Iadenmacrophages
(confirmatory)
• Aberrant location or outside the • Myometrium at least 2.5 mm from
Location
uterus the basalis
• Retrograde menstruation
• Metaplasia
• Derived from aberrant glands
• Lymphatic and vascular spread
Etiology of the basalis layer of the
• Immunologic change
endometrium
• Genetic predisposition
• Iatrogenic dissemination
• Does not respond to cyclic
• Responds to cyclic changes in
Cyclic changes changes in ovarian hormone
ovarian hormone production
production
Prevalence • Nulliparous women • Multiparous women
Symptoms • Dysmenorrhea and infertility • Dysmenorrhea and menorrhagia
• Fixed retroverted uterus with

I
• Diffuse symmetric enlargement of
posterior tenderness
Signs the uterus, 2-3 times the normal
• Nodularities at uterosacrals
size
• Ovarian cysts
• Ultrasound
• Laparoscopy
• Confirmed following histologic
Diagnosis • Confirmed following histologic
examination of the uterus after
examination of implants
hysterectomy
• Pain relief
Goals of • Pain relief • Preservation of fertility
Management • Preservation of fertility • Control abnormal uterine
bleeding
• Medical management may be less
than satisfactory
Management • Medical and Surgical
• Hysterectomy (definitive
treatment)

341
 SECTION THREE
BENIGN DISORDERS OF THE OVARIES

OVERVIEW OF BENIGN CYSTS/TUMORS OF THE OVARY

• 75% of ovarian mass in women in reproductive age are functional cysts
• Functional cysts: most common cause of simple cystic adnexal mass in the reproductive age
• Benign cystic teratoma: most common cause of complex adnexal mass
• Pregnancy: most common differential to a pelvic mass

I. GENERALCLASSIFICATION
FUNCTIONAL CYSTS I BENIGN CYSTS/TUMORS
• Follicular cysts • Dermoid cyst (mature teratoma)
• Corpus luteum cysts • Endometriomas
• Theca-lutein cysts • Fibroma
• Brenner tumor (transitional cell tumors)
• Adenofibroma & cystadenofibroma

II. BENIGN VERSUS MALIGNANT CLINICALAND ULTRASOUND FINDINGS

I BENIGN
I MALIGNANT
Mobility • Mobile • Fixed
• Solid or mixed
• Cystic
• Multilocular
• No solid components
Consistency • Multicystic
• No septations
• Nodular; papillary
• Smooth, thin capsule & septa
• Irregular, thick capsule & septa
Tumor surface • Smooth • Irregular
Lat:'erality • Unilateral • Bilateral
Size • <8 cm • >8 cm
• Ascites
Associated • Peritoneal masses
• Calcifications
features
• Lymphadenopathy

III. RISK FACTORSFOR OVARIAN CANCER

INCREASED RISK I DECREASED RISK
• Family history; BRCA-1gene • Decreased ovulatory age
• Obesity 0 Breast feeding

• Endometriosis, PID, high meat & fat diet 0OCP,aspirin, NSA!Ds

(epithelial type) 0 Increasing parity
• Smoking - mucinous epithelial type • Risk Reducing Salpingo-Oophorectomy
• Increased ovulatory age (RRSO) for high risk population or
Infertility
0 opportunistic salpingectomy during cesarean
0 Nulliparity section or hysterectomy with ovarian
Late child bearing
0 conservation
Late menopause
0

Source:Momenimovahed Z, et al. IntJ WomensHealth;2019

Societyof GynecologicOncologistsof the Philippines;2019

342
FUNCTIONAL CYSTS OF THE OVARIES
DIAGNOSIS*
ETIOPATHOGENESIS MANIFESTATIONS OBSERVATION**
(Ultrasound)
Follicular Cyst
• Most frequent cystic • Most are • Usually <8 cm • Repeat
structures in the asymptomatic • Unilateral, simple ultrasound
normal ovaries • Translucent and and unilocular in after 6-8 weeks
• Persistence of thin walled structure
dominant follicle, or • Filled with clear,
• Failure of a follicle to watery to straw
rupture during the colored fluid
follicular maturation
phase
-
Corpus Luteum Cyst
• Failure of the corpus • Halban triad: • Larger • Repeat
luteum to regress • Spotting with • Simple, unilateral ultrasound
during the luteal delay in menses and unilocular in after 6-8 weeks
phase • Unilateral pain structure
• Clinically more • Small, tender,
important than adnexal mass
follicular cysts • Smooth, red to
brown
• Gray-white if
chronic
Theca Lutein Cyst
• Least common of the • Almost always • Multicystic • Theca Lutein
three physiologic bilateral (partially solid/ will regress
ovarian cysts
• Prolonged or
excessive stimulation
by endo/exogenous
gonadotropins (e.g.,
• Massive ovaries
(;elO cm)
• Hypereactio
luteinalis (multiple
luteinized
partially cystic)
• Bilateral
after pregnancy

I
hCG) follicular cysts)
• Increased sensitivity • Honeycomb
to gonadotropins appearance
• Straw colored fluid
'Diagnosticsto request:pregnancytest, vaginalultrasound
"Laparoscopyis donefor:
• Adnexalmasses aftermenopauseor beforepuberty
• Solidadnexalmass regardlessof age
• Cysticmasses >8 cm
• Cysticmasses 5-8cm persisting>8 weeksin a menstruatingwoman

343
BENIGN OVARIAN TUMORS
I. ETIOPATHOGENESIS
~ ·,.
Egltheltal Tlimod
"' - -· -
Serous • Most frequent ovarian epithelial tumors
cystadenoma • Resembles the fallopian tubes
• Can reach enormous size
Mucinous
• Multilocular with mucoid substance within
cysadenoma
• Resembles cells of en do cervix or intestinal epithelium
• Transitional cell tumor
• Solid mass or nests of epithelial cells & a surrounding fibrous stroma
Brenner tumor
• Epithelium similar to transitional epithelium of the urinary bladder
• Epithelial cells have "coffee bean"-appearing nucleus
...
Germ Cell Tumors
• Dermoid cysts/ Mature teratoma: involve all 3 germ layers
• 80% occur in reproductive life
Benign cystic • Most common neoplasm in prepubertal female
teratoma • Rokitansky protuberance: site where most varied tissue types are
found; most common location also of malignant transformation
• Monodermal teratoma made up of thyroid tissue: struma ovarii
,~
Stromal Tumor ow ,.
• Most common benign solid tumor of the ovary
• Extremely slow growing and unilateral
• Whorled pattern on cross section
Fibroma • Meig Syndrome:
1. Ovarian Fibroma
2. Ascites
3. Hydrothorax

II. DIAGNOSTICSFORADNEXAL MASSES

DIAGNOSTIC I REMARKS
• Pregnancy Test
• Serial quantitative ~-hCGto evaluate suspected ectopic pregnancy
Basic
• CBC:elevated WBC may indicate pelvic inflammatory disease (PIO)
diagnostics
or tuba-ovarian abscess (TOA), or pelvic abscess from colonic or
appendiceal pathology
• Does not need to be measured on all premenopausal women with
Serum cancer
simple ovarian cyst on ultrasound
antigen -125
(CA-125) • Not recommended for differentiating between benign and malignant
adnexal mass
Lactate
dehydrogenase
(LDH), • Should be measured in all women under the age of 40 with complex
alpha- ovarian mass because of the likelihood of germ cell tumors
fetoprotein
(AFP) and hCG
• Transvaginal ultrasound with color Doppler imaging (primary
imaging modality): to identify specific diagnosis, differentiate from
a non-gynecologic pathologies, differentiate benign from malignant
Imaging
masses, or to evaluate extent of the disease
• CT scan and MRI: adjunct to ultrasound for uncertain or problematic
cases and to determine the extent of the disease

344
GENERAL APPROACH TO ADNEXAL MASSES
I. APPROACHTO ADNEXAL MASSES IN PREMENARCHEALCHILDREN
• A complete pediatric examination should include a complete history and thorough
inspection and palpation of the involved sites and possible related areas
• Transabdominal ultrasonography: first-line imaging modality
• Children with simple ovarian cyst <10 cm with no malignant features should be
manage expectantly (otherwise, surgery is preferred)
• Laparoscopy is preferred over open surgery in benign ovarian tumors
• For malignant diseases, surgical staging is recommended but with preservation of the
uterus and contralateral ovary even in advance disease.

Serum Markers

I 13-HCG I AFP I LDH

I CA-125

Dysgerminoma + - + -
Endodermal Sinus Tumor - + - -
Choriocarcinoma + - - -
Immature Teratoma - + + +
Embryonal Carcinoma + + - -
Source:LawrenceAE,et al. J PediatrSurg;2020

II. APPROACHTO ADNEXAL MASSES IN REPRODUCTIVE-AGEWOMEN

A. Overview of Management
CHARACTERISTICS I MANAGEMENT
r,Asymptom'!fic
- -
• Expectant management
• These cysts may be physiologic cysts and would resolve

■
Simple cysts <5 cm after a few menstrual cycles
• Repeat ultrasound during the first half of the follicular
phase (days 4-6) after 3 cycles may be done
• >50% are functional and will resolve within 2-3
menstrual cycles, repeat ultrasound after 3 months
Asymptomatic with simple • If ovarian cyst is still present at 6 months, CA-125 may
cysts 5-7 cm be requested
• lfCA-125 is <200 IU/mL and there are no suspicions
for malignancy, may opt to observe
• No consensus of cut-off size
Persistent asymptomatic
• Some recommend that a persistent asymptomatic cyst
cysts
>6 cm may be offered surgical management
Syt,lptomatic '
Symptomatic ovarian cysts
that peresent with pain or • Surgical management
pressure symptoms
~ ·111
With Suspicion of Malignancy
"' -
Any size with non-benign
ultrasound findings and/
or elevated tumor markers • Surgical management
that are highly suggestive
of malignancy
Source:lrabonI. et al. POGS;2018

345
 B. Surgical Management
0 Benign masses may be removed laparoscopically or through laparotomy
0 Ovarian cystectomy if:
• Preoperative suspicion for malignancy is low
• Mass appears benign intraoperatively
• No evidence of metastatic disease
0 Aspiration of ovarian cyst should not be done

III. APPROACH TO ADNEXAL MASSES IN POSTMENOPAUSAL WOMEN

A. Overview of Management
0 Surveillance every 3-6 months may be offered to postmenopausal women who have
adnexal masses with low risk of malignancy:
• Normal CA-125 <35 !U/mL
• Asymptomatic, simple, unilateral, unilocular simple cysts, <7 cm in diameter
0 If there is no increase in size and if the CA-125 remains normal, frequency of
surveillance may be decreased or may be done annually

B. Surgical Management if:

0 Symptomatic
0 Suspicious or persistent complex adnexal mass regardless of size
0 Asymptomatic with simple adnexal cyst >7cm in diameter

REFERENCES
!.Clinical Practice Guidelines for the Obstetrician-Gynecologist. Society of Gynecologic Oncologists of the Philippines
(Foundation), Inc. Third Edition. July 2019
2.Donnez J, Dolmans MM. Uterine fibroid management: from the present to the Future. Hum Reprod Update. 2016
Nov:22(6):665-686. doi: 10.1093/humupd/dmw023. Epub 2016 Jul 27. PMID: 27466209; PMCID:PMC5853598.
3.lrabon, I. Manaement of adnexal masses in reproductive-aged women. Clinical Practice Gudelines on Adnexal Masses.
PhilippineObstetricaland Gyneocological Society,Inc. November 2018
4.Kumar,R.,Ellenson,H, Ronnett, L., Brigette.M.. Blaustein'sPathologyof the FemaleGenitalTract. New York:Springer,2019.
$.LawrenceAE, FallatME, Hewitt G,et al. Understandingthe Valueof Tumor Markers in PediatricOvarianNeoplasms.)Pediatr
Surg. 2020;55(1 ):122-125. doi:10.1016/i.jpedsurg.2019.09.062
6.Lobo RA,GershensonDM, Lentz GM, Valea FA.ComprehensiveGynecology. 7th edition. Elsevier,2017
7.MomenimovahedZ, Tiznobaik A, Taheri S, SalehiniyaH. Ovarian cancer in the world: epidemiologyand risk factors.Int J
Womens Health. 2019;11:287-299. Published 2019 Apr 30. doi:10.2147 /IJWH.Sl 97604
8.Munro MG,CritchleyHOD,Fraser IS,FIGOMenstrual DisordersCommittee.The tvvoFIGOsystemsfor normal and abnormal
uterine bleeding symptomsand classificationof causesof abnormal uterine bleeding in the reproductiveyears: 2018
revisions. In J Gynaecol Obstet 2018; 143:393.
9.PhilippineObstenicaland Gynecological Society.ClinicalPracticeGuidelineson Myoma and AdnexalMasses,2010
10. PhilippineSocietyfor ReproductiveMedicine.ClinicalPracticeGuidelineson Endometriosis,2014
11. PhilippineSocietyfor ReproductiveMedicine.ClinicalPracticeGuidelinesfor Uterine Leiomyomas,2017
12. QuickReferenceManual on ReproductiveEndocrinologyand Infertility: 1st ed.,Diliman,QuezonCity: PhilippineSocietyof
ReproductiveEndocrinologyand Infertility, Inc.,2012
13. Rees,V.(2020, September8). EMA safetycommitteerecommendswithdrawal of ulipristalacetatemarketingauthorization.
European Pharmaceutical Review. Retrieved from: https://www.europeanpharmaceuticalreview.com/news/127776/
ema-safety-committee-recommends-withdrawal-of-ulipristal-acetate-marketing- authorisation/
14. Reinhold C,Tafazoli F, Mchio A, Wang L,Atri M, Siegelman ES, Rahaman L. Radiographies. 1999;19 Spec No:Sl47.

346
 INFECTIONS
TRACT
GENITAL
 SECTION ONE
OVERVIEW OF THE GENITAL TRACT INFECTIONS
OVERVIEW OF GENITAL TRACT INFECTIONS
• Infections of the female genital tract may include:
Sexually transmitted diseases
Endogenous infections
Iatrogenic infections

SEXUALLY TRANSMITTED DISEASES (STD)

• Refers to a variety of syndromes caused by pathogens that can be acquired and
transmitted through sexual activity

I. MAJORSTD PATHOGENSTHAT PRODUCE INFECTIONS

PREGNANCY-
ETIOLOGIC AGENT ACUTE DISEASE ASSOCIATED
I I CONDITIONS
• Ophthalmia neonatorum
Chlamydia trachomatis • Urethritis • Neonatal pneumonia
• Cervicitis • Postpartum endometritis
• Salpingitis
• Pelvic inflammatory • Prematurity
Neisseria gonorrhea disease (PID) • Septic abortion
• Neonatorum ophthalmia
• Spontaneous abortion
Treponema pal/idum • Syphilis • Stillbirth
• Congenital syphilis
Haemophilus ducreyi • N/A
Herpes simplex virus 2 • Genital ulcer • Neonatal HSV

I
(HSV-2) • Prematurity
Human papilloma virus • Congenital laryngeal
• Genital warts
(HPV) papillomatosis
Source:BrunhamRC,et al. PlenumPress;1992

II. PREVENTION METHODS

METHOD I REMARKS
• One of the most effective methods for preventing
Pre-exposure transmission of HPV
vaccination • HPV vaccination is recommended routinely and can be
administered beginning at 9 years of age
Abstinence or
mutual monogamous • Most reliable way to avoid transmission of STDs
relationship
• Highly effective in preventing HIV,HPV,and HPV-associated
Male condoms
diseases, genital herpes, hepatitis B, syphilis, and chancroid
• Female condoms
Other methods • Cervical diaphragms
• Topical microbicides and spermicides

349
ENDOGENOUS INFECTIONS
• These are infections that arise when commensal or endogenous bacteria that possess
pathogenic prerequisites attain replicative dominance
• Caused by overgrowth of organisms normally present in the genital tract of healthy
women (e.g., bacterial vaginosis or vulvovaginal candidiasis)

Commensal Microorganisms that Produce Infections

ETIOLOGIC AGENT I DISEASE I PATHOGENESIS
• Bacterial • Decrease in the number of Lactobacil/i1s
Gardnerella vagina/is
Vaginosis spp. results in decreased production
of hydrogen peroxide & acid thereby
• Vulvovaginal allowing for unrestricted growth of
Chlamydia spp
Candidiasis commensal microorganisms in the flora

IATROGENIC INFECTIONS
• Refer to infections caused by low-virulence organisms introduced to the genital tract by
medical procedures such as dilatation and curettage or JUD insertion during childbirth
• Includes infections from improperly performed procedures (e.g., unsafe abortion or poor
childbirth practices)

Common Pathogens Related to D&Cand JUDInsertion

PROCEDURE I DISEASE I PATHOGENESIS I COMPLICATIONS
• Iatrogenic introduction
• Organisms • Septic abortion
of vaginal flora in the
may invade the • Severe necrotizing
Dilatation & intrauterine cavity
myometrial infections
Curettage • Group A streprococcus
tissues & • Toxic shock syndrome
(S. pyogenes)
• C/ostridium perfringens extend to cause
parametritis,
• Vulvovaginal peritonitis &
IUD • Pelvic inflammatory
Candidiasis septicemia
insertion disease
• Actinomyces infection

350
 SECTION TWO
LOWER GENITAL TRACT INFECTIONS
BARTHOLIN GLAND CYST AND ABSCESS
• Bartholin glands (or the greater vestibular glands) located in the entrance of the vagina
(at 5 and 7 o'clock positions) secrete mucus to lubricate vulva
• Most common Bartholin masses (when the glands are obstructed) are cysts or abscesses

I. ETIOPATHOGENESIS
• Infection, trauma, mucus changes, or congenitally narrowed ducts may cause obstruction
of the Bartholin duct leading to cystic dilation of the Barthol in duct (Bartholin Cyst)
• When Bartholin cysts become infected (usually E.coli), they form a Bartholin abscess

II. MANIFESTATIONS

Cause • Polymicrobial infection of cysts

• Found in the labia majora and duct orifices are at the base of the labia
Location
minora just distal to the hymen (5 and 7 o'clock positions)
Size •l-Bcm
Laterality • Often unilateral but may be bilateral
• Tense cystic mass • Develops rapidly (2-4 days)
Signs
• Clear/white fluid • Erythema, tenderness, edema
• Acute vulvar severe pain
• Usually non-painful
Symptoms • Dyspareunia
• May be asymptomatic
• Pain during walking
Source:Lobo,et al. Comprehensive
Gynecology.
7thed. 2017

■
III. DIAGNOSIS
Differential diagnoses: mesonephric cyst, epithelial inclusion cyst
• Diagnostics:
° CBC,urinalysis, transperineal ultrasound, GS/CS of abscess
Biopsy of capsule wall for patients ;,40 years old and/or recurrent abscess
0

IV. MANAGEMENT
MANAGEMENT I INDICATION
Marsupialization • Bartholin gland abscess
(I&D) • Bartholin gland cyst in a patient less than 40 years old
• Bartholin gland cyst in a patient " 40 years old
Excision
• Recurrent abscess and/or persistent deep infection
Antibiotics
with anaerobic • Barthol in gland abscess
coverage
Source:Lobo,et al. Comprehensive
Gynecology.
7thed.2017

351
VULVAR INFECTIONS
PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
pt
Pedicu osis (hh irus pu bis o_rera bl ouse
·- -
• Most • Confined to hairy • Direct • Recommended: permethrin
contagious of areas of vulva microscopy 1% cream rinse OR
all STDs • Pubic pruritus pyrethrin with piperonyl
• Direct • Eggs (nits), lice & butoxide
transmission pepper grain feces • Alternative: malathion 0.5%
(e.g. sexual in pubic hair lotion OR ivermectin 250
contact) µg/kg body weight orally,
repeated in 7-14 days
Scab(flS(Sareop'te/scabei)
,.
-
~

• Pruritic skin • Widespread over • Microscopy • Recommended: permethrin

infection hairy parts of body using scratch 5% cream OR ivermectin
produced • Severe intermittent technique 1% lotion applied to all
by the mite itching at night (mites lack areas of the body from neck
Sarcoptes • Burrows: lateral claw down & washed off after
scabei pathognomonic legs but have 8-14 hours (repeat in 1
• Direct sign of scabies 2 triangular week if symptoms persist),
transmission infection hairy buds) OR ivermectin 200 ug/kg
via close repeated in 14 days
contact • Alternative: lindane lotion
or cream applied in a thin
layer to all areas of the body
from neck down & washed
off after 8 hours
• Antihistamines for pruritus
Molluscum Contap,to;um[Iioxvi,:us}
• Benign, mild • Asymptomatic & • Visual • Spontaneous healing within
skin disease mildly contagious inspection 6-12 months in most
due to pox • 2-Smm flesh- • Microscopy • May be excised with
virus colored, dome- of waxy treatment of base using:
• Transmission shaped papules material 0 Mansel solution

by skin-to- with central from nodule: 0 Trichloroaceic acid (TCA)

skin contact, umbilication in intra- , Cryotherapy

autoinoculation, the vulva, thighs, cytoplasmic
or fomites buttocks molluscum
bodies with
Wright or
Giemsa stain
,.-
Condyloma0Aeumihaf;ym (Humanl!ty1i119mavlr.us6,)1)
" -
• HPV 6, 11: • Genital, venereal, • Visual • Patient-applied:
associated with or anogenital inspection 0 lmiquimod cream

external genital warts • Biopsy when 0 Sinecatechins ointment

warts • Cauliflower-like lesions do , Podofilox solution or gel
• Most common lesions that can be not respond
viral STD of the asymptomatic or to therapy, • Provider-applied:
vulva, vagina, may present with condition ° Chemical (trichloroacetic
anus, cervix pain, itching worsens, or acid or bichloroacetic
• Transmission malignancy acid solution)
by direct is suspected 0 Electrocautery

contact, • HPV ° Cryotherapy

autoinoculation serotyping: 0 Surgical excision
not required
352
GENITAL ULCERS
• Defined as single or multiple vesicular, ulcerative or erosive lesions in the genital area
(e.g., vulva, perianal area)
• Usually due to infectious agents or sexually transmitted diseases

I. SYPHILIS
A. Etiopathogenesis
° Chronic complex systemic disease caused by 'lreponema pallidum (anaerobic, elongated,
tightly-wound spirochete which can penetrate the skin or mucous membrane)
0 Highest risk: women from lower socioeconomic groups, adolescents, early-onset
sexual activity, multiple sex partners
° Contagious during the primary, secondary & probably the 1st year of latent phase
0 In pregnant patients, transplacental transmission is most common

B. Manifestations
STAGE I MANIFESTATIONS
• Ulcers or chancre at the infection site
• Chancre: hallmark lesion; solitary, painless ulcer with raised, rounded
Primary
borders and uninfected base in the cervix, vagina, vulva, mouth, anus
• Usually heals spontaneously but may undergo secondary infection
• Systemic disease, skin rash, mucocutaneous lesions, lymphadenopathy
• 6 weeks to 6 months after chancre appears
Secondary • Maculopapular rash over the palms of the hands and the soles of the feet
• VuIvar lesions: mucous patches & condyloma lata associated with
painless adenopathy
• Follows secondary stage
Latent
• Positive serology without symptoms or signs of the disease
• Seen in untreated syphilis that may appear up to 20 years after
• Potentially destructive effects on the central nervous, cardiovascular,
and musculoskeletal systems
Tertiary
• Optic atrophy, tabes dorsalis, generalized paresis, aortic aneurysm

I
• Gummas: similar to a cold abscess with a necrotic center and the
obliteration of small vessels by endarteritis

C. Diagnosis
• VDRL(Venereal Disease Research Laboratory) test
Screening*
• RPR (Rapid Plasma Reagin) test
• Treponema Immobilization Test
Confirmatory • FTA-ABS(Fluorescent Treponemal Antibody-Absorption)
Tests • MHA-TP(Micro-hemagglutination Treponema pallidum)
• Darkfield microscopy: shows thin, silvery spiral motile organism
'Bothtests abovemeasureanticardiolipin
antibodies,causingpotentialfalse-positive
resultsfromotherconditions

353
 D. Management
Parenteral penicillin G is the preferred drug for all stages of syphilis
0

Treatment for latent and tertiary syphilis require a longer duration of therapy
0

Jarisch-Herxheimer reaction: acute, self-limited febrile response with headache

0

and myalgia in the 1st 24 hours after treatment of syphilis

STAGE
I RECOMMENDED
I ALTERNATIVES*

Primary, • Doxycycline 100 mg orally BID

Secondary, & • Benzathine Penicillin G 2.4 for 2 weeks, OR
Early Latent million units IM single dose • Tetracycline 500 mg orally QID
Phase for 2 weeks
• Benzathine Penicillin G 7.2 • Doxycycline 100 mg orally BID
Late Latent
million units total (2.4 million for 4 weeks OR
and Tertiary
units lM at once a week intervals • Tetracycline 500 mg orally QID
Phase
x 3 doses) for 4 weeks
• Aqueous crystalline penicillin G • Procaine penicillin G 2.4
Neurosyphilis, 18-24 million units per day, million units IM once daily,
Ocular or administered as 3-4 million units PLUS
Otosyphilis IV every 4 hours or continuous • Probenecid 500 mg orally 4
infusion for 10-14 days times/day, both for 10-14 days
'Givento penicillin-allergic
patients

II. CHANCROID
A. Etiopathogenesis
0 Bacterial STD caused by Haemophilus ducreyi (highly contagious small gram-
negative rod, "school of fish" in microscopy)
0 Sexually transmitted, acute, ulcerative disease of the vulva

B. Manifestations
Soft chancre: painful and tender ulcers with ragged edges
0

Tender inguinal adenopathy

0

Genital ulcers of chancroid facilitate the transmission of HIV infection

0

C. CDCCriteria for Probable Diagnosis ofChancroid:

0 Patient has one or more painful genital ulcers
° Clinical presentation, appearance of genital ulcers and, if present, regional
lymphadenopathy are typical for chancroid
0 Patient has no evidence of T. pal/idum infection by darkfield examination of ulcer
exudate or by a serologic test for syphilis done at least 7 days after onset of ulcers
0 An HSV PCR test or HSV culture performed on the ulcer exudate is negative

D. Management
Azithromycin 1 g PO in a single dose, OR
0

° Ceftriaxone 250 mg IM in a single dose, OR

° Ciprofloxacin 500 mg BID x 3 days, OR
Erythromycin base 500 mg TID x 7 days
0

Sources:CDCST!TreatmentGuidelines,2021
Lobo,et al. ComprehensiveGynecology.
7th ed. 2017

354
Ill. GENITALHERPES
A. Etiopathogenesis
0 Most prevalent genital ulcer disease
° Chronic, life-long viral infection caused by herpes simplex virus (HSV) 1 or 2, which
can enter sensory nerve endings
• HSV-1: genital herpes can be caused by oral-genital sexual practices
• HSV-2: causes primarily genital lesions
0 Recurrent, highly contagious
0 More severe in women compared to men

B. Manifestations
0 Paresthesia of the vulvar skin
0 Papule and vesicle formation
0 Severe vulvar pain, tenderness and inguinal adenopathy
0 General malaise and fever
0 Recurrence may be related to the onset of menstrual period or emotional stress
0 Prodrome: sacroneuralgia, vu Ivar burning, tenderness and pruritus for a few hours
to 5 days before vesicle formation
0 HSV resides in a latent phase in the dorsal root ganglia of S2, S3 and S4

C. Diagnosis
0 Viral culture positive in primary episodes
0 Nucleic acid amplification test (NAAT): most accurate and sensitive
0 Western blot assay for antibodies to HSV: most specific method for diagnosing
recurrent, unrecognized or subclinical herpes
0 HSV culture, ELISA and lmmunoblot test

D. Management
INDICATION
I VALACYCLOVIR
I ACYCLOVIR
I FAMCICLOVIR
First clinical • 1000 mg BID x 7-10 • 400 mg TID x 7-10 • 250 mg TID x 7-10
episode days days* days
• 125 mg BID x 5

I
• 800 mg BID x 5 days, OR
• 1000 mg daily x 5
Recurrent days, OR • 1000 mg BID x 1
days, OR
episodes • 800 mg TID x 2 day, OR
• 500 mg BID x 3 days
days** • 500 mg once then
250 mg BID x 2 days

Daily • 500 mg daily, OR

suppressive • 1000 mg daily if>lO • 400 mg BID • 250 mg BID
therapy recurrences per year
'Acyclovir,200 mg 5x a day is also effectivebut not recommendedbecause of the frequencyof dosing
"Acyclovir,400 mg TIOis also effectivebut not recommendedbecause of the frequencyof dosing
Sources:CDCSTITreatmentGuidelines,2021
Lobo,et al. ComprehensiveGynecology.7th ed. 2017

355
IV. LYMPHOGRANULOMA VENEREUM (LGV)
A. Etiopathogenesis
0 STD characterized by skin lesions followed by regional lymphadenopathy in the groin
° Chronic infection of lymphatic tissue, mostly affecting the vulva
° Caused by Chlamydia trachomatis

B. Manifestations
0 Most common manifestation among heterosexuals is tender inguinal and/or femoral
lymphadenopathy that is typically unilateral (buboes)
PHASE I DESCRIPTION
Primary • Shallow painless ulcer of the vestibule or labia, which resolves
Infection spontaneously
Secondary • Bubo: painful adenopathy in inguinal and perirectal areas
Infection • Groove sign: enlarged lymph node, tender and matted
• Formation of multiple draining sinuses and fistula
Tertiary • Extensive destruction of external genitalia & a no rectal region leading
Infection to extensive scarring which can lead to elephantiasis, multiple fistulas,
stricture formation of the anal canal and rectum

C. Diagnosis
° Culture, direct immunofluorescence or nucleic acid detection of C. trachomatisofpus
or aspirate from an infected node
° Complement fixation antibody titer >l:64 is indicative of infection

D. Management
0 Doxycycline 100 mg BID x 21 days
0 Alternative:
• Azithromycin 1 gram PO once weekly for 3 weeks (then do test of cure with C.
trachomatisNAAT 4 weeks after completion of treatment), OR
• Erythromycin base 500 mg QID x 21 days

V. DONOVANOSIS (GRANULOMA INGUINALE)

A. Etiopathogenesis
° Chronic, slowly progressive, ulcerative, bacterial infection of the skin and
subcutaneous tissue of the vulva
0 Sexual or non-sexual contact
0 Not highly contagious and chronic exposure is necessary to contract the disease
0 Due to Klebsiella granulomatosis (a Gram negative, non-motile, encapsulated rods)

B. Manifestations
0 Initially appears as asymptomatic nodule which ulcerates (beefy red ulcer with fresh
granulation tissue), coalesce, and eventually destroy the normal vu Ivar architecture (if
untreated)
0 Subcutaneous involvement (i.e., pseudobubo)
0 Secondary bacterial infection

C. Diagnosis
0 Microscopy using silver stain: Donovan bodies (clusters of dark-staining bacteria with
a bipolar or safety-pin appearance)

D. Management
0 Azithromycin 1 gm orally once weekly, OR 500 mg once daily for at least three weeks
and until all lesions completely heal
0 Alternative regimens (minimum treatment duration 3 weeks and until lesions have
completely healed)
• Doxycycline 100 mg BID
• Erythromycin base 500 mg QID
• Trimethoprim-sulfamethoxazole 800 mg/160 mg BID

Source:CDC.STITreatment
Guidelines,
2021
356
- -
_ ULCERS
LYMPHOGRANULOMA
CHANCROID GENITAL HERPES
VENEREUM (LGV)
mapallidum • Haemophilus ducreyi • HSVl/ HSVZ • Chlamydia trachomatis (Ll, LZ,L3) • Klebsiell,

eks • 1-14 days • 2-7 days • 3 days - 6 weeks • 1-4 wee!<

:ontact • Asymptomatic shedding

• Sexual contact • Sexual contact • Sexual co
acental • Sexual contact

• Papule or pustule • Vesicle • Pa pule, pustule or vesicle • Papule

• Usually multiple, may

one • Multiple, may coalesce • Usually one • Variable
coalesce

• 2-20 • 1-2 • 2-10 • Variable

demarcated, • Undermined, • Erythematous • Elevated • Elevated

,r oval • Ragged, irregular • Sharp • Round or oval • Irregular

cial or deep • Excavated • Superficial • Superficial or deep • Elevated

1, non-
• Purulent • Serous, erythematous • Variable • Red and,
It

• Soft • None • Occasionally Firm • Firm

I • Usually very tender• • Common • Variable • Uncomm1

iscrete, • Tender, may suppurate, • Tender (buboes), may suppurate

• Firm, tender, bilateral • Pseudobt
11 usually unilateral • Multiloculated, unilateral

• Antigen detection by
Id direct • Direct lmmunostaining ELISA • Giemsas1
• Gram Stain • lmmunoperoxide
>florescence rapid Assay • Tissuesn
staining and ELISA

eyi"(painfululcers) Source:Lobo,et al. Comprehensive

Gynecology.
7thed.2017;HolmesKK,et al. Sexuallytransmit!

-
VAGINITIS
Overview of Differentials for Vaginitis based on Vaginal Discharge*

FEATURE
I NORMAL
I
BACTERIAL
VAGINOSIS
I
TRICHOMONIASIS ICANDIDIASIS

• White, • Thin,whitish • Yellow, frothy • White, thick,

floccular gray homogenous discharge with or curdy
Appearance
• Gray,milky discharge, without vaginal or • "Cottage
white, creamy sometimes frothy cervical erythema cheese-like"

pH <4.5 >4.5 >4.5 <4.5

Amine odor (-) + (-) (-)

Clue cells (-) + (-) (-)
Trichomonads (-) (-) + (-)
Mycelia (-) (-) (-) +
'Typicaldischarge of cervicitis(discussed in the next section) is purulentor mucopurulent(yellowish)

I. BACTERIALVAGINOSIS(BV)
A. Etiopathogenesis
0 Polymicrobial syndrome resulting from replacement of the normal hydrogen peroxide
producing Lactobacillus spin the vagina with high concentrations of anaerobic bacteria
(e.g., Gardnerel/a vagina/is)
0 BV is sexually associated rather than transmitted
0 Routine treatment of sexual partner(s) not recommended

B. Manifestations/Diagnosis:
0 BV is the most prevalent cause of vaginal discharge or malodor
° Can be diagnosed using a clinical criteria or Gram stain

l. Amsel (Clinica11 Criteria (3 out of4 features):

• Vaginal fluid pH >4.5
• Clue cells (e.g., vaginal epithelial cells studded with adherent coccobacilli) on a gram
stain or wet mount of vaginal discharge
• Homogenous, thin, milky white discharge
• Whiff test: fishy odor when 10% KOH is added to the vaginal discharge
Source:AmselR, et al. AmJ Med;1983

2. Gram Stain
• Considered the gold standard laboratory method for diagnosing BV
• Used to determine the relative concentration of the following organisms:
• Lactobacilli (i.e., long Gram-positive rods) are decreased
• Gram-negative and Gram-variable rods & cocci (i.e., G. vagina/is, Prevotel/a,
Porphyromonas, and peptostreptococc,)
• Curved Gram-negative rods (i.e., Mobiluncus)

C. Management

• Metronidazole 500 mg/tab BID x 7 days, OR

Recommended • Metronidazole gel, 1 full applicator (5 g) intravaginally OD x 5 days, OR
Regimen • Clindamycin cream 2%, 1 full applicator (5 g) intravaginally at
bedtime x 7 days

• Clindamycin 300 mg orally 2 times/day for 7 days, OR

• Clindamycin ovules 100 mg intravaginally once at bedtime for 3 days, OR
Alternative
• Secnidazole 2 g oral granules in a single dose, OR
Regimen
• Tinidazole 2 g orally once daily for 2 days, OR
• Tinidazole 1 g orally once daily for 5 days
Source: CDC.STITreatmentGuidelines,2021

358
II. TRICHOMONIASIS
A. Etiopathogenesis
0 Due to Trichomonas vagina/is (tetra flagellated motile protozoan)
0 Most prevalent nonviral STD

B. Manifestations
0 Most are asymptomatic (70%)
0 Green-yellow frothy vaginal discharge with offensive odor
0 "Strawberry" cervix or colpitis macularis (punctate hemorrhages)
0 Dyspareunia
0 Vulvovaginal soreness and itching
, Dysuria and frequency

C. Diagnosis
0 NAAT(Nucleic Acid Amplification Test): the new gold standard
° Culture (previously considered as the gold standard)
0 Trichomonads seen on wet mount: most common method because of convenience

D. Management
Trichomoniasis among women: metronidazole 500 mg PO BID x 7 days
0

Trichomoniasis among men: metronidazole 2 g orally in a single dose

0

Alternative regimen for men and women: tinidazole 2g PO in a single dose

0

III. VULVOVAGINALCANDIDIASIS (VVC)

A. Etiopathogenesis
0 Usually caused by Candida albicans (90%) or other species
0 VVC is not sexually transmitted

B. Manifestations
Pruritus (primary symptom)
0

Erythema, edema, excoriation

0

Abnormal vaginal discharge (white, curdy discharge)

0

C. Diagnosis
0 Hyphal elements on KOH smear (wet preparation)
0Gram stain with yeast hyphae or pseudohyphae
° Culture with Nickerson or Sabouraud

~~~~----1
~- Management: Recommended Re,qimen for Vulvova,qinal Candidiasis
Over-the-Counter Intravaginal Agents
• Clotrimazole 1% cream 5 g intravaginally daily for 7-14 days, OR
• Clotrimazole 2% cream 5 g intravaginally daily for 3 days, OR
• Miconazole 2% cream 5 g intravaginally daily for 7 days, OR
• Miconazole 4% cream 5 g intravaginally daily for 3 days, OR
• Miconazole 100 mg vaginal suppository one suppository daily for 7 days, OR
• Miconazole 200 mg vaginal suppository one suppository for 3 days, OR
• Miconazole 1,200 mg vaginal suppository one suppository for 1 day, OR
• Tioconazole 6.5% ointment 5 g intravaginally in a single application
Uncomplicated
vvc Prescription Intravaginal Agents
• Butoconazole 2% cream (single-dose bioadhesive product) 5 g
intravaginally in a single application, OR
• Terconazole 0.4% cream 5 g intravaginally daily for 7 days, OR
• Terconazole 0.8% cream 5 g intravaginally daily for 3 days, OR
• Terconazole 80 mg vaginal suppository one suppository daily for 3 days

Oral Agent
• Fluconazole 150 mg orally in a single dose
Sources:Source:CDC.STITrealment
Guidelines,
2021
Lobo,et al. Comprehensive
Gynecology.
7thed.2017

359
 .
Complicated VVC u ..
y

• Initial therapy: 7-14 days of topical therapy or a 100-mg,

Recurrent VVC
(>4 episodes of symptomatic VVC
within 1 year}
SevereVVC
(i.e., extensive vulvar erythema,
edema, excoriation, and fissure
formation)
Non-albicans VVC
Women with diabetes,
immunocompromising
conditions (e.g., HIV infection),
underlying immunodeficiency,
or immunosuppressive therapy
(e.g., corticosteroids)
150-mg, or 200-mg oral dose offluconazole every 3rd
day, for a total of 3 doses (day 1, 4, & 7)
• Suppressive maintenance therapy: oral fluconazole (100
mg, 150 mg or 200 mg dose} weekly for 6 months
• 7-14 days of topical azole, or
• 150mg Fluconazole in two sequential doses (second
dose 72 hours after initial dose)
• Longer duration of therapy (7-14 days) with a non-
fluconazole azole regimen (oral or topical)
• If with recurrence: Boric acid 600mg acid in a gelatin
capsule administered vaginally one daily x 3 weeks
• Efforts to correct modifiable conditions, and
• Prolonged (7-14 days) conventional treatment
Sources:Source:CDC.ST!TreatmentGuidelines,
2021
Lobo,et al. Comprehensive
Gynecology.
7thed.2017

CERVICITIS
I. ETIOPATHOGENESIS
• Refers to inflammation of the uterine cervix, which primarily affects the columnar
epithelial cells of the endocervical glands or the squamous epithelium of the ectocervix
• Sexually transmitted disease
• Typical pathogens of cervicitis include:
• Chlamydia trachomatis
• Neisseria gonorrhea
• In most cases, no organism is isolated
• Cervicitis can ascend and cause endometritis or pelvic inflammatory disease (PIO)

II. MANIFESTATIONS
• Frequently asymptomatic, but some complain of vaginal discharge/bleeding, dyspareunia,
or an edematous/hypertrophic cervix
• Two major diagnostic signs characterize cervicitis:
• Purulent or mucopurulent endocervical exudate visible in the endocervical canal or on
a endocervical swab specimen
Sustained endocervical bleeding easily induced by gentle passage of a cotton swab
through the cervical os

IV. DIAGNOSIS
• Leukorrhea (>10 WBC/high-power field (hpf) on microscopy of vaginal fluid: associated
with chlamydia! and gonococcal infection of the cervix
• Gram negative intracellular diplococci on gram stain: specific for gonococcal cervicitis
• Nucleic acid amplification testing (NAAT) for testing for chlamydia & gonorrhea

GENERAL CRITERIA I ALTERNATIVE CRITERIA

• Gross visualization of yellow
mucopurulent material on a white
cotton swab
• Presence of;;:10 PMN leukocytes per
hpf on gram-stained smears obtained
from the endocervix
• Erythema and edema in an area of cervical
ectopy or associated with bleeding secondary
to endocervical ulceration
• Friability when endocervical smear is obtained
• Increased vaginal discharge and
intermenstrual vaginal bleeding
Source:Lobo,et al. Comprehensive
Gynecology.7thed.2017
Centersfor DiseaseControlandPrevention.
MMWR;2015
360
V. APPROACHTO CERVICITISDEPENDING ON ETIOLOGY
• When mucopurulent cervicitis is clinically diagnosed, empirical therapy for C. trachomatis
(most common cause) is recommended for women at risk
• Risk factors include:
Age <25 years old (sexually active)
0 New or multiple sex partners
0 Unprotected sexual contact
• If prevalence of N. gonorrhea in the population is >5%, concurrent therapy for
N. gonorrhea is also indicated
• If presumptive treatment is deferred, NAAT for both C. trachomatis and N. gonorrhea is
necessary

I Neisseria Gonorrhea* I Chlamydia Trachomatis

• Gram negative intracellular
diplococci found in epithelium of
the genitourinary tract, rectum,
Description pharynx or the eye • Obligatory intracellular organism
• Localized acute infection
resulting to bacteremia or
disseminated infection

Manifestation • Vaginal discharge • Usually asymptomatic

• Gold standard: NAAT
• Culture (i.e. Thayer Martin)
• Gram-stained smear of the
• Gold standard: NAAT
Diagnosis endocervical swab: gram
• Culture
negative intracellular diplococci
• Enzyme immunoassay
• Nucleic Acid Hybridization Test
Recommended • Ceftriaxone 500 mg IM in a • Doxycycline 100 mg orally BID x
regimen single dose (SD)** 7 days
• Azithromycin, lg orally SD, OR
• Levofloxacin, 500 mg orally daily
• Gentamicin 240 mg IM SD, PLUS

■
Alternative x 7 days
• Azithromycin 2 g orally SD, OR
regimens • Pregnant: Azithromycin 1 g orally
• Cefixime 800 mg orally SD
SD, OR Amoxicillin 500 mg orally
TID x 7 days
•1fchlamydia!infectionhas not been excluded,providersshouldalso treat forchlamydiawithdoxycycline100 mg
orally2 times/dayfor 7 days
.. For persons weighing2'150kg, 1 g ceftriaxoneshouldbe administered
Source:CDC.STITreatmentGuidelines,2021

361
 SECTION THREE
PELVIC INFLAMMATORY DISEASE
OVERVIEW OF PELVIC INFLAMMATORY DISEASE (PID)
• PID refers to infection in the upper genital tract (e.g., uterus, fallopian tubes, ovaries) not
due to pregnancy or intraperitoneal pelvic operations
• Sexually transmitted
• Although some are asymptomatic, others are not diagnosed because patient or health-
care provider fails to recognize implications of even mild symptoms (e.g., infertility)

I. ETIOPATHOGENESIS
A. Pathophysiology

• Includes a combination of endometritis,

salpingitis, tuboovarian abscess, and
pelvic peritonitis
• Ascending polymicrobial infection due to
Penton1t1s
cervical microorganisms (e.g.,
ont1s C. trachomatis and N. gonorrhea) or the
Endometnt1s vaginal microflora
Cervicitis

B. Pathophysiology
• Results from ascending infection from the bacterial flora of the vagina
Acute PID
and cervix
(<30 days)
• Mostly commonly secondary to N.gonorrhea and C. trachomatis.
ChronicPID • Associated with Mycobacterium tuberculosis or Actinomyces

C. Risk Factors
0 History of STDs and PIO 0 Multiple sexual partners
0 Early age at first coitus 0 IUD use
0 Young age <25 years old (sexually active) 0 Induced abortion
0 Lack of barrier contraception use 0 lmmunocompromised state

D. Etiologic Agents
0 Majority are due to sexually transmitted infections (e.g., N. gonorrhea, C. trachomatis)
0 Microorganisms of the vaginal flora (e.g., anaerobes, G. vagina/is, H. influenzae, enteric
Gram-negative rods, Streptococcus agalactiae)
0 Others: cytomegalovirus, M. hominis, U urealyticum, M. genitalium

II. MANIFESTATIONS

• Most frequent symptom of acute PIO: new-onset lower abdominal and

pelvic pain
Symptoms
• Non-specific symptoms: hypogastric pain, abnormal vaginal bleeding or
discharge, dyspareunia, fever
• Ectopic pregnancy
• Infertility
Sequalae
• Chronic pelvic pain
• Subsequent PID

• Persistent PIO may lead to development of tuboovarian abscess

(inflammatory mass involving fallopian tube, ovary, & adjacent structures)
Complications
• Fitz-Hugh Curtis Syndrome: some develop symptoms of perihepatic
inflammation (e.g., RUQ pain/tenderness, pleuritic pain)

362
III. DIAGNOSIS

I CRITERIA
Minimum criteria • Uterine tenderness or
(presumptive • Adnexal tenderness or
diagnosis)* • Cervical motion tenderness

• Oral temperature >38°C

• Abnormal cervical or vaginal discharge (mucopurulent)
• Presence of abundant WBCs on microscopy of vaginal secretions
Additional
• Elevated erythrocyte sedimentation rate (ESR)
criteria**
• Elevated (-reactive protein (CRP)
• Laboratory documentation of cervical infection with N. gonorrhea
or C. trachomatis

• Histopathologic evidence of endometritis on endometrial biopsy

Specific
• Transvaginal sonography or MRI showing thickened fluid-filled
(definitive)
tubes, with or without free pelvic fluid or tuboovarian complex
criteria
• Laparoscopic abnormalities consistent with PIO
'Empiricaltreatment of PIDshould be initiatedin sexuallyactive youngwomen and others at riskfor STDs if above
minimumcriteriaare present and no other causes(s) for the illnesscan be identifiable
"Additionalcriteriaenhance specificityof the minimumclinicalcriteriaand support the diagnosis

MANAGEMENT OF PIO
• Regimens must provide empiric, broad spectrum coverage of likely pathogens
• All regimens used should be effective against N. gonorrhea & C. trachomatis because
negative endocervical screening for these does not rule out upper genital infections
Treatment should be initiated as soon as the presumptive diagnosis has been made

I. MEDICALMANAGEMENT
ROUTE
I RECOMMENDATION
Intramus~ular/Qral Regimen*
• Ceftriaxone 500 mg IM in a single dose (SD)** PLUS doxycycline 100 mg PO BID x 14 days

■
with metronidazole 500 mg PO BID x 14 days, OR
• Cefoxitin 2 g IM as SD & probenecid 1 g PO concurrently as SD PLUS doxycycline 100 mg
PO BID x 14 days with metronidazole 500 mg PO BID x 14 days, OR
• Other parenteral 3rd-generation cephalosporins (e.g., ceftizoxime or cefotaxime) PLUS
doxycyc!ine 100 mg PO BID x 14 days with metronidazole 500 mg PO BID x 14 days
-
fareqteral Regimen***
• Ceftriaxone 1 g IV every 24 hrs PLUS doxycycline 100 mg PO or IV
every 12 hrs PLUS metronidazole 500 mg PO or IV every 12 hrs, OR
Recommended • Cefotetan 2 g IV every 12 hrs PLUS doxycycline 100 mg PO or IV every
regimen 12 hrs, OR
• Cefoxitin 2 g IV every 6 hrs PLUS doxycycline 100 mg PO or IV every
12 hrs

• Ampicillin/sulbactam 3 g IV every 6 hrs PLUS doxycycline 100 mg PO

or IV every 12 hrs, OR
Alternative
• Clindamycin 900 mg IV every 8 hrs PLUS gentamicin loading dose
regimen
IV or IM (2 mg/kg), then maintenance dose (1.5 mg/kg) every 8 hrs
(gentamicin single daily dosing at 3-5 mg/kg can be substituted)
'IM or oral therapy can be considered for mild-to-moderateacute PIO
"For persons 2'150kg (-300 lbs.) withdocumentedgonococcalinfection,1 gm of ceftriaxoneshould be given
'"Oral therapy can be initiatedwithin24-48 hours of improvementwithparenteraltherapy
Source: CDC.STITreatmentGuidelines,2021

363
II. CRITERIA FOR HOSPITALIZATION
• Surgical emergencies (e.g., appendicitis) cannot be excluded
• Tuboovarian abscess
• Pregnancy
• Severe illness, nausea and vomiting, or high fever
• Unable to follow or tolerate an outpatient oral regimen
• No clinical response to oral antimicrobial therapy

III. SURGICALMANAGEMENT
• Considered if there is clinical deterioration or no improvement after 24-48 hours of
antibiotics & is restricted to life-threatening infections, ruptured tuba-ovarian abscesses,
or persistent and symptomatic masses.
• Options include:
0 Ultrasound-guided aspiration of abscess
0 Laparoscopic-guided drainage of abscess cavities or salpingo-oophorectomy or
salpingectomy (goal: uterine & ovarian preservation to maintain fertility)
0 Pelvic clean up (i.e. THBSO): for completed family size

IV. FOLLOWUP
• Clinical improvement should be apparent within 72 hours of initiation of therapy
• If patient is responding, she should be examined 4-6 weeks after therapy to assess
resolution of clinical symptoms and establish a posttreatment baseline
• If no improvement within 72 hours after outpatient IM/oral therapy, hospitalization,
assessment of the antimicrobial regimen & consideration of diagnostic laparoscopy for
alternative diagnoses or for definitive surgical management are recommended
• All diagnosed with chlamydia! or gonococcal PIO should be retested 3 months after
treatment

IV. TESTING OF PARTNERS

• Partners within 60 days of onset of symptoms should be evaluated, tested and
presumptively treated for gonorrhea and chlamydia
• If last sexual contact is more than 60 days, test and treat the most recent partner

REFERENCES
1.Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, Centers for Disease Control and Prevention,
2015. MMWR Recomm Rep 2015;64
2.Amsel R, Totten PA, Spiegel CA, et al. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations.
Am J Med 1983;74:14-22
3.SchwebkeJR.Hillier SL, Sobel JD, et al. Validity of the vaginal gram stain for the diagnosisof bacterial vaginosis.Obstet
Gynecol 1996;88(4 Pt 1):573-6.
4.Powell AM, Nyrijesy P.Acute cervicitis. Uptodate. Available online https://www.uptodate.com/contents/acute-cervicitis.
Accessed on July 4, 2021
5.Brunham RC, Embree JE. Sexually transmitted diseases: current and future dimensions of the problem in the third world.
In: Germain A, Holmes KK, Piot P.Wasserheit JN,editors. Reproductivetract infections:global impact and priorities for
women's reproductivehealth. New York: Plenum Press;1992
6.Lobo RA,GershensonOM, Lentz GM, Valea FA.Comprehensivegynecology.7th edition. Elsevier,2016
7.Bryan Larsen, Gilles R. G. Monif. Understandingthe Bacterial Flora of the FemaleGenital Tract
8.Clinical Infectious Diseases, Volume 32, Issue 4, 15 February 2001, Pages e69-e77, https://doi.org/10.1086/318710
9.Centers for Disease Control and Prevention. SexuallyTransmtiied Infections Treatment Guidelines, 2021. \V\.,,,...,.cdc.gov.
Accessed September 23, 2021
10. Holmes KK.Mardh PA,Sparling PF,et al. Sexually transmitted diseases, 2nd ed, New York: McGraq-Hill; 1990

364
PELVIC
FLOOR
 SECTION ONE
OVERVIEW OF ANATOMY & PHYSIOLOGY OF PELVIC FLOOR

ANATOMY OF THE PELVIC FLOOR

I. PELVICFLOOR MUSCLES
• Muscles of the pelvic floor, particularly the levator ani muscles, provide support to the
pelvic visceral organs (e.g., bladde1; uterus, vagina, rectum) & play an important role in
urinary and sexual function
• Pelvic floor muscles have a constant baseline tone (except during voiding, defecation, and
Valsalva maneuver) to help close the urethral/anal sphincters and provide constant support
• Disorders of the pelvic floor may involve the muscles, ligaments, or tissues of the lower pelvis

-..-..-..---;,,1+- Coccygeus

Puborectalis
lliococcygeus
I
Levator
ani
~"':::-77---- Pubococcygeus

• Pelvic diaphragm
o Levator ani (pubococcygeus, puborectalis, iliococcygeus)
o Coccygeus
• Perinea! membrane
• Deep perinea! pouch

II. THREE LEVELSOF PELVICSUPPORT

• All levels of vaginal support are connected through a continuous endopelvic fascia
support network

■
Vaginal cuff

Uterosacral ligament

Sacrospinousligament

Obturator internus

Arcustendineus

Levell~
Level 2

'-'~c:
Level 3 ,~~';:•;"'''""

Symphysis
pubis
Vesical
neck

• There are three integrated levels of vaginal support (discussed on the next page)
• These supports may be affected by congenital anatomic weaknesses, stresses of
childbearing, injury, surgical damage, and straining
367
 • Uterosacral ligament • Loss of support contributes
Apical
I Support
(strongest uterine support) to prolapse of uterus and/or
• Cardinal ligament vaginal apex
• Anterior: pubocervical or • Loss of support contributes to
Midvaginal
II Support
pubovesical fascia anterior vaginal wall prolapse
• Posterior: rectovaginal fascia (cystocele)
• Anterior: pubourethral
Distal • Loss of support results in distal
III Support
ligament
rectocele or perinea! descent
• Posterior: perinea! body
Source:Stepp,KJ,et al.A MosbyElsevier,Philadelphia
2007

PHYSIOLOGY OF VOIDING (MICTURITION)

• Micturition is both a voluntary and involuntary event.
• The central nervous system (CNS) controls storage and voiding.
• Continence is determined by the balance between forces that maintain urethral closure
and those that affect detrusor function
• For the involuntary event, storage and voiding of urine are mediated by both the
parasympathetic and sympathetic nervous system
0 Parasympathetic system (via acetylcholine): stimulates receptors in the bladder wall
to activate detrusor contraction
0 Sympathetic system: leads to bladder relaxation
I. VOIDING AND STORAGE
PARAMETER
I VOIDING
I STORAGE

Innervation • Parasympathetic • Sympathetic

Main nerve • Pelvic nerve
Action mediated • Sacral-spinal cord: S2-S4
via (sacral micturition center)
,.
• Acetylcholine stimulates
muscarinic receptors (M3) of
Neurotransmitter
the detrusor muscle, causing it
to contract.
• lntravesical pressure (from
contraction of the detrusor
muscle) exceeds the urethral
closure pressure
Effect
• Voluntary relaxation of the
external urethral sphincter
from the cerebral cortex allows
for urine passage
• Hypogastric nerve
• Thoracolumbar cord: Tl0-L2
• Norepinephrine stimulates
the ~3 adrenoceptors in the
fund us & body and the al
adrenoceptors of bladder neck
• Urethral closure pressure
exceeds intravesical pressure
• Stimulation of the ~3
adrenoreceptors causes
detrusor relaxation
• Stimulation of al
adrenoceptors cause
contraction of bladder neck
• Impulses travel via pudenda!
nerve to nicotinic receptors in
the external urethral sphincter
causing contraction and
preventing urine flow

II. URETHRAL SPHINCTER INNERVATION

• Internal sphincter is involuntary as controlled by the pelvic and hypogastric nerves.
• External sphincter is under voluntary control (somatic outflow to the urethra is mediated
by the pudenda) nerve)
368
 SECTION TWO
PELVIC ORGAN PROLAPSE (POP)
ETIOPATHOGENESIS AND MANIFESTATIONS OF POP
• POP is the herniation of pelvic organs to or beyond the vaginal walls due to failure of
various anatomic structures to support the pelvic viscera
• It refers to an abnormal descent of the pelvic organs from their
• attachments to the pelvis

I. PATHOPHYSIOLOGY
• The descent of one or more of the pelvic organs:
Anterior compartment prolapse: cystocele, urethrocele
0 Posterior compartment prolapse: rectocele, perinea! descent
Apical compartment prolapse: uterine prolapse, enterocoele, vaginal vault prolapse

• See description of the normal anatomy

Normal
in Section 1

• Anterior vaginal wall has descended

from its original anatomical position
o Cystocoele (descent of the
bladder): defect of the pubocervical
Anterior
or pubovesical fascia
Compartment
o Urethrocele (descent of the urethra):
Prolapse
defect of the pubourethral ligament
o Cystourethrocele: if both the
urethra and urinary bladder have
prolapsed into the vaginal introitus

Posterior
• Posterior vaginal wall has descended
from its original anatomical position
o Rectocoele (descent of the rectum):
■
Compartment defect of rectovaginal fascia
Prolapse o Perinea! descent: detachment
of the perinea! body from the
rectovaginal fascia

• Elongation of posterior cul-de-sac

along the rectovaginal septum
• Vaginalapex (cervixor post-hysterectomy
vaginal cuff) has descended from its
Apical original anatomical position
Compartment o Uterine prolapse: defect of the
Prolapse uterosacral and cardinal ligaments
o Enterocoele: elongation of the cul-
de-sac with small bowel trapped
within a peritoneal sac
o Vault prolapse: usually occurs post-
hysterectomy
369
II. RISK FACTORS FOR POP
• Multiparity, vaginal childbirth • Genetic factors, race (Caucasians)
• Obesity • Musculoskeletal disease
• Increased intraabdominal pressure (e.g., Marfan syndrome, Ehlers-Danlos)
(e.g., chronic cough, asthma, COPD) • Smoking
• Aging • Trauma, prior surgery
Menopause • Neurologic injury
Hypoestrogenism

III. MANIFESTATIONS
A. Symptoms of POP:

Bulge/pressure • Vaginal or pelvic pressure

symptoms • Sensation or a bulge or something falling out of the vagina
• Irritative: frequency, urgency, nocturia, urinary incontinence
Lower urinary (stress and urge)
tract symptoms • Voiding difficulty: weak stream, straining to void, sensation of
incomplete emptying, splinting
• Constipation, straining to defecate, incomplete evacuation,
Bowel
digitation (finger-like protuberance), or fecal incontinence (solid,
symptoms
liquid, flatus)
Sexual • Interference with sexual activity
Symptoms • Dyspareunia

B. Physical Examination
0 The unequivocal diagnosis or pelvic organ prolapse can only be made on physical
examination
0 Each compartment of the vagina (anterior, posterior, and apex) must be inspected and
evaluated separately to define the true nature and degree of prolapse

PELVIC ORGAN PROLAPSE QUANTIFICATION SYSTEM (POP-Q)

• The International Continence Society (!CS), the American Urogynecologic Society, and the
Society of Gynecologic Surgeons published a consensus document for an objective system
to describe POP
• Each aspect of POP,uterine (cervical) prolapse, anterior vaginal wall (compartment),
posterior vaginal wall (compartment), vaginal vault (cuff scar) prolapse should be subject
to a clinical staging

STEP 1: PRE-PROCEDURE CONSIDERATIONS

• Perform examination with an empty bladder and rectum
• Position the patient where the utmost magnitude of the prolapse is shown (e.g., supine,
standing, lithotomy, left lateral)

STEP 2: PERFORM MEASUREMENTS USING THE "POINTS TO REMEMBER"

• There are six defined points (Aa, Ba, C, D, Ap, Bp) used to report the extent of descent or
prolapse of the anterior vaginal wall, vaginal apex, and posterior wall
• Positions of these points are measured in relation to the hymen:
0 If the point descends to the hymen it is measured as 0 cm
If the point remains above the hymen it is described as negative integers (in cm)
If the point descends beyond the hymen it is described as positive integers (in cm)

370
A. Locations of the Six Defined Points when Prolapse if Fully Reduced:

gh

POINT
I DESCRIPTION
Anterior Vaginal Wall
• Point at the midline of the anterior vaginal wall 3 cm proximal to the
external urethral meatus
PointAa
• Position of Point Aa relative to the hymen may be -3 (indicating no
anterior vaginal POP) to +3 cm (indicating a full prolapse)
• Point that refers to the most superior location of the front vaginal wall
Point Ba 0 Can coexist with Aa (-3 cm) in a woman with no anterior prolapse
0 Can coexist with point Cina woman with full prolapse
Upper Vagina
• Lowest edge of the cervix or the vaginal cuff
Pointe
• This location identifies if the cervix is descending
PointD • It is the topmost point of the posterior vaginal wall
Posterior Vaginal Wall
- - -
■
• Point located in the midline of the posterior vaginal wall 3 cm
PointAp proximal to the hymen.
• Position of Point Ap relative to the hymen is -3 to +3 cm
• Point at the most distal position of any part of upper posterior vaginal
PointBp
wall (between vaginal cuff or posterior vaginal fornix and Point Ap)

B. Other Descriptive Landmarks to Measure

POINT I DESCRIPTION
• Measured from the middle of the external urethral meatus to the
Genital
posterior margin of the hymen
hiatus (GH)
• Larger distance may indicate laxity in the opening of the puborectalis muscle
Total vaginal • Length of the vagina from posterior fornix to hymen when Point C or D
length (TVL) is reduced to its full normal position
Perinea) body • Measured from the posterior margin of the hymen to the mid-anal
(PB) opening

371
STEP 3: RECORD THE MEASUREMENTS
Anterior Anterior Cervix or
wall wall cuff

Aa Ba • The above measurements are recorded

C
on a 3 x 3 grid (seen on the left)
Total • There are three further descriptive
Genital Perinea)
vaginal measurements, which are also recorded
hiatus body
length independent of the hymen (gH, pB, TVL)
• All points are recorded during maximal
gH pB TVL Valsalva or cough, except for point TVL
(which is recorded at rest with the
Posterior Posterior Posterior
wall wall fornix prolapse reduced)

Ap Bp D

STEP 4: STAGING OF THE PROLAPSE

• Depending on the measurements, prolapse of each of the compartments is staged based
on its relationship to the hymen

1980 1996

STAGE! STAGEII STAGEIII STAGEIV

• The most distal • Prolapse is between • Prolapse is > 1 cm • Complete eversion
prolapse is > 1 cm 1 cm above and below the hymen, or eversion to within
above (inside) the 1 cm below the but no value is 2 cm of the TYL of
hymen hymen ~TVL -2 cm (i.e., not the lower genital
• Points Aa, Ba, C, D, • Any of points Aa, Ba, completely everted) tract is demonstrate
Ap, and Bp are all C, D, Ap, and Bp has • Any of points Aa, Ba, • Any of points Aa, Ba,
less than -1 cm a value of -1 cm and C, D, Ap, Bp is ~+ 2cm C, D, Ap, Bp is
+lcm and ~TVL -3cm ~TVL-Zcm

Measuring POPStaging
• POP-Qemploysthehymenas the pointof referenceandassigneda valueof 0
• Pointsabovethe hymenaredesignated(-)measuredin cm
• Pointsbelowthe hymenaredesignated(+)measuredin cm
POPis consideredsymptomaticwhenthe leadingedgeof theprolapseis at or beyondthelevelof thehymen(i.e.,
~stage2 POP-Q).
Source:HaylenBT,et al. Int Urogynecol
J, 2010andMadhuC, et al. NeurourolUrodyn,2018
372
MANAGEMENT OF POP
I. CONSERVATIVEMANAGEMENT
• Diet (i.e. increase fluid and fiber intake)
• Non-weight bearing exercises
Lifestyle
• Weight loss
modifications
• Avoid activities that can increase intra-abdominal pressure
• Control medical co-morbidities (i.e. chronic cough, constipation, obesity)
• Also called "Kegel Exercises"
• Involves isolation and repetitive contraction of pelvic floor muscles
Pelvic floor over a period of time
muscle training • There is no consensus regarding the frequency and number of pelvic
(PFMT) floor contractions but the usual advice is as follows:
8-10 contractions, 10 seconds per contraction, 3x a day
• Ideally coached by physiotherapist for symptomatic women

II. SURGICALMANAGEMENT
• Goals are for symptom relief, treatment of pelvic support defects, maintenance of
bladder /bowel and sexual function, and prevention of recurrence

TYPE OF
PROLAPSE

Anterior·Compdrtmept Prolapse
• Cystocoele • Anterior colporrhaphy • Burch colposuspension
• Urethrocoele • Transvaginal mesh interposition • Sacrocolpopexy with anterior
• Cystourethrocele mesh interposition
. "'
Posterior Compartment Prolapse -
• Rectocoele • Posterior colporrhaphy • Sacrocolpopexy
• Perinea! descent • Transvaginal mesh interposition
Apical Compar.tmen~Prolapse
• Bilateral Ileococcygeal Fascia • Sacrohysteropexy
(BICF) or prespinous fixation • Sacrocolpopexy
• Uterine prolapse • Sacrospinous ligament fixation • Uterosacral fixation/
• Enterocoele
• Vault prolapse
• Uterosacral ligament fixation/
suspension
• McCalls culdoplasty
• Obliterative (i.e. Colpocleisis)
suspension
• Culdoplasty (Moschowitz/
Halban)
II

373
III. VAGINALPESSARY
• Made of soft PVCor silicone material
• May be offered to all women regardless of site or severity of prolapse
• Two types: support pessaries and space-occupying pessaries
Choice is usually based on experience and trial and error

A. Support Pessaries
Lie along the vaginal axis providing a supportive shelf for the descending pelvic organs
0

Generally easier to insert, allow sexual intercourse and are associated with less
0

discharge or vaginal irritation than space-occupying pessaries

RING PESSARY I GEHRUNG PESSARY I HODGE PESSARY

• For all types and stages of
prolapse (usually for 1st
and 2nd degree)
• Usually first choice
because of ease of
insertion and removal
• For cystoceles and
rectoceles with or without
uterine descent
• ·For mild cystoceles in
woJTienwith a narrow
pubic arch
• For correcting a
retroverted uterus

B. Space-Occupying Pessaries
CUBE PESSARY I DONUT PESSARY I GELHORN PESSARY

• For advanced prolapse • For advanced prolapse • For advanced prolapse

especially if the perinea! with decreased perinea!
support is lax support
Source:ScottFarrell.Springer-Verlag;
2006

374
 SECTION THREE
URINARY INCONTINENCE
OVERVIEW OF URINARY INCONTINENCE
• Involuntary loss (or leakage) of urine that is objectively demonstrable and is a social or
hygienic problem
• Risk factors include increasing age, obesity, high parity, history of vaginal delivery, and
family history

I. ETIOPATHOGENESISAND TYPES OF INCONTINENCE

TYPE I PATHOPHYSIOLOGY I CAUSES/RISKS

• Involuntary loss of urine thru
an intact urethra, secondary • Activities of increased
to increased intraabdominal abdominal pressure (e.g., heavy
pressure in the absence of bladder lifting, straining, constipation,
Stress or detrusor contraction chronic cough)
(Urinary)
• Mechanism of SUI: • Childbirth
Incontinence
(SUI)*
0 Urethral hypermobility from • Aging
insufficient pelvic floor support • Menopause
0 Internal sphincter deficiency • Obesity
from loss of muscular tone that • Smoking
normally keeps urethra closed
• Aging
• Me_nopause
Urgency • Neurologic disorders (e.g.,
• Involuntary loss of urine due to
(Urinary) spinal cord injury)
uninhibited detrusor contractions
lncoqtinence • Diabetes
(or an overactive bladder)
(UUI)* • Childbirth
• Pelvic surgery (i.e. post-
hysterectomy)
• Involuntary loss of urine
• Detrusor underactivity: low
characterized by incomplete
estrogen state, peripheral
bladder emptying
• Can be due to: neuropathy (i.e. diabetes), .~.
Overflow damage to the efferent nerves
0 Detrusor underactivity: detrusor
Incontinence of the spinal cord (i.e. multiple
areflexia or hypotonic bladder
sclerosis)
(from impaired contractility of
• Bladder outlet obstruction:
the detrusor muscle)
tumors, advanced POP
, Bladder outlet obstruction
• Inability to reach the restroom
due to factors unrelated to the • Decreased mobility post-
Functional
urinary tract surgery
Incontinence
• Requires intact urinary storage • Decreased manual dexte_rity
and voiding function

• Loss of urine thru abnormal • Surgery

communications between the • Prolonged obstructed labor
Extra-urethral
reproductive and urinary tract • Irradiation
Incontinence
• Manifests with genitourinary • Tumors
fistulae • Trauma
'Mixedincontinence:
womenwith-symptoms
of bothstressandurgency
incontinence

375
II. MANIFESTATIONS
TYPE I MANIFESTATIONS
Stress • Urine loss during coughing, laughing, sneezing
Incontinence • There is no urge to urinate prior to the leakage
• Frequent, small volume voids that keeps the patient up at night
Urgency • Symptoms may worsen after taking a diuretic
Incontinence • Patient may have a strong urge to void with an inability to make it to the
bathroom in time
• Presents with continuous urinary leakage or dribbling in the setting of
incomplete bladder emptying
Overflow • Due to detrusor muscle underactivity: loss of urine with no warning and
Incontinence occurs with a change in position
• Due to bladder outlet obstruction: often with stress or urgency
symptoms with a sensation of incomplete emptying

Ill. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Urinalysis and culture when appropriate
• Kidneys/ureters/bladder (KUB) ultrasound
Basic tests
• Pelvic floor ultrasound
• KUB-intravenous pyelogram (to diagnose genito-urinary fistula)
• Position patient in the lithotomy position with a moderately full bladder
Cough stress
• Tell tlie patient to cough / bear down
test
• Observe for urine loss per urethra
• Objective measurement of severity of urinary leakage by measuring the
Pad test number of pads used over a certain period of time
• Does not determine the type of urinary leakage
• Measures the pressure volume.relationship of the bladder
• Examples of different urodynamic studies:
Urodynamic
Office cystometry
0
studies
Multi-channel urodynamic studies
0

Video urodynamics
0
-
• Visualization of the urethral lumen using a fiber optic-illuminated rigid
Urethroscopy
scopes
• Visualization of the urinary bladder cavity using a fiber optic-
Cystoscopy
illuminated rigid scopes
• Aids in determining the location of the fistula
• First dye: take rifampicin PO 4-6 hours or inject indigo carmine IV prior
to the procedure
• Second dye: insert 3 gauze pads inside the vagina and methylene blue
introduced retrograde in to the urethra thru a Foleycatheter until the
Two-Dye Test sense of urgency is felt
• Interpretation of tests:
0Proximal and/or middle gauze turns blue: vesicovaginal fistula
0Proximal gauze turns orange: ureterovaginal fistula
0Distal gauze turns blue: urethrovaginal fistula or spillage of the dye
thru the urethral meatus

376
MANAGEMENT OF URINARY INCONTINENCE
I. BASIC MANAGEMENT
DIAPPERS
• Delirium
• Infection
Modification • Atrophic urethritis and/or vaginitis
of transient • Pharmaceuticals (i.e. antihistamines, decongestants, ACE-inhibitors,
causes of diuretics)
incontinence • Psychologic disorders
• Excessive urine output (i.e. hyperglycemia)
• Restricted mobility
• Stool impaction
• Dietary changes
Lifestyle
• Smoking cessation
modification
. • Weight loss
• Topical vaginal estrogen: for peri- or postmenopausal women with
vaginal atrophy in the presence of concomitant stress or urgency
Estrogen incontinence
• Oral estrogen +/- progestin: for peri- or postmenopausal women with
vaginal atrophy, in the presence of other systemic climacteric symptoms

II. MANAGEMENT BASED ON TYPE OF INCONTINENCE

TYPES OF
INCONTINENCE
I REMARKS

• Primary treatment is surgical:

0 Mid-urethral sling (tension-free vaginal tape [TVT] or
transobturator tape [TOT])
0 Pubovaginal sling
0 Burch colposuspension
Stress 0 Periurethral bulking agents
Incontinence • Conservative management:
° Kegel exercises
° Knack maneuver: voluntary contraction of the pelvic floor before

■
and during a cough
0 Bladder training: timed voids (i.e. every 2-3 hours)
0 Pessary
• Primary treatment is medical
0 Anticholiner.gics
0 p3-adrenergic receptor agonists
Urgency
• Kegel exercise
Incontinence
• Bladder training
• Biofeedback: pressure sensors are placed inside the urethra, vagina
and rectum
Mixed Urinary
• Address the more pressing symptom
Incontinence
Overflow • Address the cause of the detrusor underactivity or the bladder
Incontinence obstruction
Functional • Modify the physical environment (i.e. grab bars in bathroom, bedside
Incontinence commodes)
-
Extra-urethral • Prolonged catheterization for the smaller genito-urinary fistula
Incontinence • Surgical repair for genito-urinary fistula

377
REFERENCES
1.Abrams P, Andersson KE, Apostolidis A, Birder L, Bliss D, Brubaker L, et al. 6th International Consultation on Incontinence
Recommendations of the International Scientific Committee: Evaluation and treatment of urinary incontinence, pelvic
organ prolapse, and faecal incontinence. Neurourol Urodyn 2018 Sep;37(7):2271·2272.
2.Bent AE, Cundiff GW, Swift SE. Ostergard's Urogynecology and Pelvic Floor Dysfunction. 6th Ed. Philadelphia: Lippincott
Williams & Wilkins (LWWJ; 2007.
3.Culbertson S, Davis AM, Nonsurgical Management of Urinary Incontinence in Women. JAMA.2017 Jan;317(!):79-80.
4.DuBeau CE, Kuchel GA,Johnson T 2nd, et al. Incontinence in the frail elderly: report from the 4th International Consultation
on Incontinence. Neurourol Urodyn. 2010;29(1):165.
S.DuBeau CE, Kuchel GA, Johnson T, et al .. Incontinence in the frail elderly. In: Incontinence, 4th ed., Abrams P, Cardozo L,
Khoury S, Wein A. (Eds), Health Publications Ltd, Paris 2009. p.961.
6.Effective Health Care Program. Nonsurgical Treatments for Urinary Incontinence in Adult Women: Diagnosis and
Comparative Effectiveness. Agency for Healthcare Research Quality 2012. Available at: http://effectivehealthcare.ahrq.
gov /ehc/products/169 /1021/CER36_Urinary-lncontinence_execsumm.pdf (Accessed on November 19, 2012).
7.Haylen BT,De Ridder D, rreeman RM, et al. An International Urogynecological Association (IUGA)/lnternational Continence
Society (ICS) joint repo1t on the terminology for female pelvic floor dysfunction. Int Urogyneco\ ]. 2010;21:S-26
8.Haylen BT, Maher CF, Barber MD, et al. Erratum to: An International Urogynecological Association (IUGA)/lntemational
Continence Society (ICS) joint report on the terminology for female pelvic organ prolapse (POP). Int Urogynecol J.
2016;27:655-684
9.Haylen BT, Maher CF,Barber MD, Camargo SFM, Dandolu V, Digesu A, Goldman HB, Huser M, Milani A, Moran P.Schaer GN,
Withagen Ml. International Urogynecological Association (IUGA) / International Continence Society (!CS) Joint Report on
the Tem1inology for pelvic organ prolapse (POP). Int Urogynecol ).2016, 27(2):165-194; Erratum,2016, 27(4): 655-684;
Neurourol Urodyn,2016,35(2):137-168.
10. Lobo RA, Gershenson OM, Lentz GM,Valea FA Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
11. Madhu C, Swift S, Moloney-Geany S, Drake MJ. How to use the pelvic organ prolapse quantification (POP-Q) system?
Neurourol Urodyn 20!8;37:S39-43
12. POGSClinical Practice Guidelines on Rcconstructive and Reproductive Surgery in Gynecology. (2013)
13. Prodigalidad-Jabson L1; Amin-Ong A], Jose JB, Ocampo MS, Chan LL, Luna MTC and Sison JM, POGS Clinical Practice
Guidelines on Urogynecology. !st Ed. (2010).
14. Richter HE, Burgio KL, Brubaker L, Nygaard IE, Ye W. Weidner A. Bradley CS, Handa VL, Borello-France D, Goode PS,
Zyczynski H, Lukacz ES, Schaffer ], Barber M, Meikle S, Spino C, Pelvic Floor Disorders Nenvork Continence pessary
compared with behavioral therapy or combined therapy for stress incontinence: a randomized controlled trial. Obstet
Gynecol. 2010;115(3):609.
15. Scott Farrell, editor. Pessaries in clinical practice.London: Springer-Verlag; 2006.
16. Stepp, KJ, Walters, MD. Anatomy of the lower urinary tract, rectum, and pelvic floor. In: Urogynecology and
Reconstructive Pelvic Surgery, 3rd ed., Walters, MD, Karram, MM (Eds), Mosby Elsevier, Philadelphia 2007

378
CONGENITAL
ANOMALIES
OFTHE
FEMALE
REPRODUCTIVE
TRACT

~ OVERVIEW OF THE CONGENITAL ANOMALIES

0 CONGENITAL ANOMALIES
1. AFS Class I: Agenesis
OF THE UTERUS

2. AFS Class II: Unicornuate Uterus

3. AFS Class Ill: Uterine Didelphys
4. AFS Class IV: Bicornuate Uterus
5. AFS Class V: Septate Uterus
6. AFS Class VI: Arcuate Uterus
7. AFS Class VII: Diethylstillbestrol Related Anomalies

0 CONGENITAL ANOMALIES OF THE VAGINA AND VULVA

1. Longitudinal Vaginal Septum
2. Transverse Vaginal Septum
3. Vaginal Atresia
4. lmperforate Hymen
5. Microperforate Hymen
6. Labial Hypertrophy
 SECTION ONE
OVERVIEW OF THE CONGENITAL ANOMALIES

OVERVIEW OF THE CONGENITAL ANOMALIES

• These anomalies are usually diagnosed only after the onset of puberty
• Ovaries are unaffected in patients who have normal endocrine and oocyte functions
because the ovaries are derived from the gonadal ridge
• Patients have an age-appropriate sexual development and normal looking external genitalia

I. INCIDENCE
• Actual incidence is unknown due to underreporting or misreporting
• Incidence reported to be generally around 0.1-3.5%
• Mean incidence of uterine malformations was 4.3% for the general population
• Incidence of Mullerian duct anomalies in women with reproductive problems is 3 to 6%
0 Women with recurrent abortions have an incidence of 5-10%
0 Women having third-trimester miscarriages have a higher incidence ofMullerian defect

II. EMBRYOGENESIS
A. Formation of the Uterus and Vagina
0Mullerian ducts (paramesonephric ducts) & the urogenital sinus are the embryonic
precursors of the female reproductive tract
• Upper 1/3 of the paired Mullerian ducts become the bilateral fallopian tubes
• Lower 2/3 fuse & form the uterine corpus, cervix, and superior aspect of vagina
• Lower vagina differentiates from the primordial urogenital sinus
0Normal development of the female reproductive tract involves a series of processes
of differentiation, migration, fusion, & canalization of the Mullerian system
0Mullerian ducts are believed to embryologically merge in a caudal-cranial direction

Fallopian tube

Uterine

I
Mullerian
(paramesonephrlc)
duct caudal tip

Urogenital
sinus

• Upper third of vagina and

• At 13 weeks, the
the fornices are formed
sinovaginal bulbs have
by canalization of the
• At 9 weeks, the uterine begun to grow out of
paramesonephric tissue
septum has disappeared the pelvic part of the
• Lower third of the vagina is
urogenital sinus and form
formed by canalization of
a solid plate
the sinovaginal bulbs
Source:LangmanJ, MedicalEmbryology,
4th ed,Williams& Wilkins,Baltimore,1981
LauferMR,et al. Uptodate

381
 B. Consequential Mullerian Anomalies Upon Interruption of these Processes
PROCESS AFFECTED
I DEFECT

• Aplasia/agenesis
Organogenesis defects • Hypoplasia
• Unicornuate uterus
• Bicornuate uterus
Fusion defects
• Uterine didelphys
Resorption/canalization • Septate uterus
defects • Arcuate uterus

III. PATHOGENESIS
• Etiology of Mullerian tract anomalies is unknown
• Multifactorial patterns of inheritance and teratogens (e.g., diethylstilbestrol) have
been implicated
• Other congenital abnormalities have been associated with Mullerian duct defects
• Urinary tract anomalies
• Skeletal abnormalities
• Cardiac defects
• Auditory deficits

IV. MANIFESTATIONS
• Obstructive anomalies present earlier with menstrual disorders
• Non-obstructive types may manifest later with fertility and obstetric difficulties

V. DIAGNOSIS
• Asymptomatic patients are diagnosed incidentally
• Diagnostic imaging & minimally invasive procedures are needed for diagnosis

DIAGNOSTIC
I REMARKS
• Keytool to differentiate between a septate & a bicornuate uterus
Ultrasound • Determines presence/absence of a cervix
• Evaluate kidneys of patients with Mullerian anomalies
• Provides better information about interior contour of the
Hysterosalpingography uterine cavity (but not the external contour)
(HSG} • Determines patency of fallopian tubes
• Cannot distinguish between septate and bicornuate uteri
• Accurate delineation of both internal and external uterine
Magnetic resonance contours
imaging (MRI) • Differentiates septate from bicornuate uteri
• Determines presence/absence of a cervix

VI. OVERVIEW OF MANAGEMENT

• The decision to correct Mullerian duct anomalies depends mainly on the patient's
symptomatology
• Providing an outflow tract for menstruation and establishing sexual functions are the
more frequent indications for the surgical correction of obstructive vaginal defects
• Surgery for the reconstruction of the uterus is contemplated if patients identified with
these fusion defects encounter difficulties in conceiving or bringing a pregnancy to term
• Timing of these corrective procedures depends on when the symptoms become apparent;
otherwise, these defects are better left untouched in cases of incidental diagnosis.

382
 SECTION TWO
CONGENITAL ANOMALIES OF THE UTERUS

AMERICAN FERTILITY SOCIETY CLASSIFICATION

• Most widely used is the American Fertility Society (AFS) Classification: limits itself to
Mullerian anomalies according to the major uterine anatomic defects
• The urogenital anomalies of the vagina like vaginal atresia, transverse vaginal septum and
imperforate hymen are not included in the classification (but discussed in the next section)

CLASS I DIAGRAM I DESCRIPTION

Vaginal Cervical Fundal

• Various degrees of
hypoplasia/agenesis of the
Class I:
upper reproductive tract
Hypoplasia/
agenesis (the uterus, cervix, and
upper two-thirds portion
of the vagina)
Tubal Combined Complete

• Characterized by arrest in
development of one of the
Class II:
Miillerian ducts, resulting
Unicornuate
in either a present or
absent rudimentary horn
Non•communicating No horn

• Complete failure of fusion

of both Miillerian ducts
Class Ill:
• Horns both well-developed
Didelphys
• Results in two separate
hemiuteri and cervices
Complete Partial
• Incomplete non-fusion of
Class IV: the Miillerian ducts
Bicornuate • Result in two hemiuteri
and a single cervix

■
Complete Partial

Class V:
Septate

T ~
~
1/,
• Failure of resorption of
midline septum

Class VI:
Arcuate ~ I , • Mild endometrial
indentation along the
uterine fundus

• Combination of
features post-exposure
Class VU: to diethylstilbestrol
DES-related (hypoplasia, T-shaped
uterine cavity, abnormal
cervical forms)
Source:TheAFSclassifications.
FertilSteril1988
383
CONGENITAL ANOMALIES OF THE UTERUS
• Congenital uterine anomalies (CUA's) may cause pelvic pain, abnormal bleeding at time of
menarche, recurrent pregnancy loss, or preterm delivery
• MRI is the gold standard for the diagnosis of these abnormalities
• General pathogenesis
0 Hypoplasia/agenesis (AFS I) and unicornuate (AFS 11):failure of one or both MUllerian
ducts to develop
Didelphys [AFS Ill) and bicornuate (AFS IV): failure ofmidline fusion
Septate (AFS VJand arcuate (AFS VI): failure of resorption of the midline septum

PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS

I MANAGEMENT

AFSCIass:I Viag,'!a IAgenesis

• Characterized by • Presents with • Ultrasound/MRI: • Frank procedure:
the congenital amenorrhea (second see description use of graduated
absence of the most common below cylinders pressed
superior two- cause of primary • MKRH is on to the vaginal
thirds of the amenorrhea) distinguished dimple to create a
vaginal canal • Mayer-Rokitansky- from androgen functional vagina
with or without a Kuster-Hauser insensitivity • Surgery:
functional uterus Syndrome [MRKH): syndrome through 0 Mcindoe
• Often coexist failure of uterus & karyotyping procedure
with uroglogic vagina to develop 0 MRKH: 46, XX 0 Pratts
anomalies (15- properly in those ° Complete androgen vaginoplasty
40%) & skeletal with normal insensitivity 0 Williams vuvlo-
anomalies (12- ovarian function & syndrome: 46, XY vaginoplasty
50%) external genitalia , Vecchietti
procedure
0 Vaginal
pull-through
procedure
Subtypes 11 - ..
• MRKH: absence of • Absence of uterus • Creation of
Complete vaginal both upper vagina on imaging neovagina for
agenesis (90%) & uterus sexual function
• Amenorrhea
• May have a • May show functional • Creation of
functional uterus endometrium on neovagina for
• Cervix,upper vagina, imaging sexual function
Partial vaginal or both are absent and for menstrual
agenesis • Hematometra, egress
cryptomenorrhea
• Cyclical, suprapubic
pain

384
 PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS
I MANAGEMENT

AFS Class II: Unicornuate Uterus

• Formed when • Pelvic pain due • Ultrasound: • Excision of

only one of the to hematometra useful to identify rudimentary
two Mullerian (cryptomenorrhea) rudimentary horns horn: done only
ducts develops or endometriosis • HSG:only one when there is
normally (sequela) fallopian tube is an associated
• Often with a • Those without visualized and rudimentary
rudimentary a rudimentary uterine volume is horn with
horn which may horn can be reduced an active
or may not have asymptomatic • MRI: more sensitive endometrial
a functional • Obstetric outcomes • !VP: done to lining present
endometrium generally poor detect urologic • Surgery not
(e.g., spontaneous abnormalities indicated when
abortion, preterm rudimentary
birth) horn is absent or
lacks a functional
endometrium
• If pregnancy
occurs in
the non-
communicating
horn, it is treated
like an ectopic
pregnancy
- - -
AFS l!ilass lll: Uterine Qii!elp,hys (or Double Uterus}

• Occurs when • Usually • Speculum exam: • If with obstructed

midline fusion asymptomatic, reveals two cervices hemivagina
of the Mullerian unless with an unless one side is (i.e., in WHWS):
ducts does not obstruction obstructed by a excision of
take place (rare • Fertility usually not transverse vaginal obstructing
defect) affected septum, usually vaginal septum
• Composed of two • Spontaneous appreciated as a to remove the
separate uteri abortion rate is unilateral fluctuant hematometra
and endocervical high: 40% intravaginal mass and prevent
canals (i.e., • Wunderlich- • Ultrasound and MRI: retrograde
duplication of Herlyn-Werner reveals two separate menstrual flow
reproductive
structures)
• Each hemiuteri
has its own
fallopian tube
Syndrome (WHWS)
or obstructed
hemivagina
and ipsilateral
renal agenesis
uterine horns each
with their own
cervix
• Renal ultrasound
or IVP: to exclude
• Uterine
unification, rarely
done
• Removal of
non-obstructing
I
and are both (OHVIRA):patients other urogenital longitudinal
functionally with unilateral anomalies vaginal septum
capable of obstruction on a case-to-case
pregnancy complain of basis
• Longitudinally dysmenorrhea
divided vaginal &commonly
canal is variably a associated with
component ipsilateral renal
agenesis & ureteral
agenesis

385
 PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS
I MANAGEMENT
AFS Class IV: Bicomuate Uterus ~

• Occurs when • Usually • Ultrasound: two • Bicornuate uterus

the Mullerian with normal separated upper by itself is not
ducts fail to fuse menstruation endometrial cavities an indication for
cephalad before with no difficulty and an indented uterine repair
the unification is conceiving fundal contour (by unless associated
completed • Preterm delivery >l cm) with poor
• Results in a rate is 60% • MRI: demonstrates obstetric history
cervical canal, two uterine bodies with no other
a lower uterine and a single cervix identifiable cause
cavity, and a with externally • Strassman
partitioned upper concave uterine Procedure
endometrial fund us (metroplasty):
cavity with an • HSG:V-shaped removal of fundal
externally cleaved configuration of cleavage by wedge
uterine fundus the uterine cavity, resection followed
but will not reveal by uniting the 2
external appearance uteri using layered
of the uterus suturing along
• Diagnostic the thickness
laparoscopy: heart- of the exposed
shaped uterine myometrium
fundus externally to form a single
uterine cavity
AFS Class V: Septa& Uterus

• Outcome of • May be partial or • Similar to a • Asymptomatic

incomplete complete bicornuate uterus uterine septum:
resorption of the • Complete: if it • Ultrasound: no intervention
combined medial extends down to two separated necessary
walls of the the internal os endometrial cavities • Candidates
Mullerian ducts and divides the • HSG or for excision
after longitudinal endometrial cavity hysteroscopy: of septum
fusion has taken completely into two V-shaped uterine (metroplasty):
placed • Does not cavity recurrent
• Most common significantly affect • MRI: demonstration spontaneous
Mullerian the ability to of normal fundal abortions, 2nd
anomaly conceive, but is contour can reliably trimester losses,
associated with differentiate a or histories of
poor reproductive septate uterus from preterm delivery
outcomes a bicornuate uterus • Standard of care:
• Spontaneous • Laparoscopy: same hysteroscopic
abortion rates up as MRI metroplasty with
to 75% attributed microscissors,
to implantation in a electrocautery, or
poorly vascularized laser performed
septum transcervically

386
 PATHOGENESIS
I MANIFESTATIONS
I DIAGNOSIS
I MANAGEMENT

AFS Class VI:Arcuate Uterus

• Mild form of • Usually • Most commonly • Managed
bicornuate uterus asymptomatic seen anomaly on similarly as
or septate uterus • Least associated HSG septate uterus
• May actually be a with adverse • Small midline notch only in patients
normal variant obstetrical is appreciated at with a poor
outcomes the fundal aspect in reproductive
the radio-opacified history
uterine cavity
:AFSClass VII:Diethylstilbestrol (DES) Related Anomalies
'
• DES: synthetic • T-shaped • Examination of • Anomalies are
estrogen endometrial cavity cervix and vagina to not amenable
prescribed in the • Widened lower exclude structural to surgical
past for recurrent uterine segment changes management
pregnancy loss, • Midfundal • HSG:structural • Cervical cerclage
premature constrictions changes involving is indicated
delivery, and • Hypoplastic uterus the cervix indicates in cases of
other pregnancy • Cervical structural high likelihood of pregnancies
complications abnormalities presence of uterine
• Banned after • Associate with poor anomaly (86%)
association with obstetric outcome
vaginal clear cell
adenocarcinoma
and various
abnormalities
!VP:intravenouspyelography
HSG:hysterosalpingogram

387
 SECTION THREE
CONGENITAL ANOMALIES OF THE VAGINA AND VULVA

DIFFERENTIALS FOR ANOMALIES OF THE OUTFLOW TRACT

IMPERFORATE HYMEN I TRANSVERSE VAGINAL I

SEPTUM
VAGINAL ATRESIA

Pathogenesis

• Membrane resulting
from the fusion between • Urogenital sinus fails
• Urogenital membrane
the vaginal plate and to canalize to form the
that fails to develop an
the caudal aspect of the inferior one-third of the
opening.
Mullerian ducts fails to vagina.
resorb

Physical Examination Findings

• Normal hymen with • No bulge or tense

• Bluish bulging membrane
shortened vagina and membrane
at the introitus
slight bulge • Acute tenting of
• Increased bulge with
• Slight indentation on hematocolpos on rectal
valsalva
rectal exam exam

• Occurs when •Maybe an • Speculum • Asymptomatic: no

the distal ends incidental finding examination intervention
of the Mullerian is enough to • Surgical
ducts fail to fuse visually diagnose transection:
properly a longitudinal indicated when
• A fibrous septum vaginal septum septum interferes
lined with • Ultrasound, CT with coitus or
epithelium divides scan, or MRI: vaginal childbirth
the vagina into confirm presence
a right and left of concomitant
canal. uterine anomalies

388
 PATHOGENESIS IMANIFESTATIONS I DIAGNOSIS
I MANAGEMENT

Vaginal Atresia/Distal Vaginal Agenesis

• Occurs when the • Primary • Diagnosis is made • Vaginal pull-
urogenital sinus amenorrhea and primarily through through
fails to canalize to cyclical hypogastric imaging procedure:
form the inferior pain associated • Obliterated part of excision of the
one-third of the with an enlarged the vagina is the fibrous tissue and
vagina. uterus palpable lower-third dissection until
• The Mullerian suprapubically • Upper segment the upper vagina
structures are • When blood fills of the vagina and is reached and
normal, but fibrous the vagina and uterine cavity then the mucosa is
tissue completely the uterus, it may distended with pulled downward
replaces the spill through the accumulated to connect to the
inferior segment fallopian tubes and menstrual blood hymenal ring
of the vagina. into the peritoneal • If patency
• Mostly isolated cavity. is sustained
anomaly,but • Sequela: after surgical
some maybe endometriosis correction, the
a component patient may get
ofautosomal pregnant
syndrome with • Hysterectomy:
anomalies of failure to maintain
the middle ear patency after
ossicle and renal repeated surgical
dysgenesis interventions
Transverse Vaginal Septum ('CVS)
-
• Forms when • Undetected until the • Transabdominal • Excision:
the membrane time of menarche ultrasound of the to prevent
resulting from the • Rarely presents pelvis: preliminary impediment to
fusion between in neonates work up the external flow
the vaginal plate with obstructed • MRI: determine of menstruation
and the caudal mucocolpos that the location and and to sexual
aspect of the causes urinary or thickness of the intercourse
Mullerian ducts rectal obstruction vaginal septum • Before menarche,
fails to resorb • After menarche, • Work-up to it should only
• Can be located presentation varies diagnose presence be excised when
anywhere along whether the TVS of associated necessary to drain
the length of the
vaginal canal:
upper third (46%),
mid vagina (40%),
is complete or
incomplete
• Complete
TVS: primary
congenital
anomalies
troublesome
mucocolpos
• The surgical
approach to TVS
I
and inferior vagina amenorrhea causing excision depends
(14%) outflow tract on the thickness
• Occasionally obstruction and location of the
associated • Incomplete TVS: septum
with urologic occasional passage • When septum is
anomalies of menstural flow, thick and area to
• Also associated but may present appose is too large,
with other with hemotocolpos split thickness
structural defects: & foul smelling graft may be used
imperforate anus, discharge
bicornuate uterus, • Sequela:
coarctation of the endometriosis
aorta, atrial septa!
defect, spine
malformation
389
CONGENITAL ANOMALIES OF THE VULVA

PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS

I MANAGEMENT

Imper/orate Hymen
• The urogenital • Often is not • Note of thin • Hymenotomy:
membrane that diagnosed until bluish membrane incision without
failed to develop an adolescent that bulges out suturing
an opening. reports primary of the vagina on ° For infants with
• Obstruct the amenorrhea examination of the mucocolpos
vaginal canal and cyclical introitus • Hymenectomy:
causing fluid hypogastric pain • Suprapubic membrane excised
accumulation • Retrograde ultrasound: fluid with edges sutured
amd bulging of menstruation filled vagina , For post-
the hymen out • Sequela: extending to the menarcheal girls
of the introitus endometriosis uterine cavity
into a thin-walled • May present with
protuberance mucocolpos in
infants
Microperforate Hy1tien
• The opening is • Periodically, • Examination of the • Hymenotomy or
much smaller menstrual flow introitus hymenectomy
than the normal escapes • Pelvic ultrasound
hymenal orifice • Hematocolpos may may be needed
also develop
• May complain
of foul-smelling
vaginal discharge

Labial Hypertrophy
• No clear cause • Labial hypertrophy
• Some are born usually affects the
with large labia, labia minora
while others • May be unilateral
develop it in the or bilateral
reproductive age • Mostly
asymptomatic
but may cause
irritation and pain
• Usual complaint:
aesthetic
• Examination of the • Asymptomatic: no
vulva treatment
• Reassurance that it
is a normal variant
• Labiaplasty: if
with discomfort
or is pulled into
the vagina during
intercourse

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Philadelphia, Pa: JB Lippincott Williams & Wilkins; 2003:705.
32. Sarto, GE, Simpson, JL. Abnormalities of the Mullerian and Wollfian Duct systems. Birth defects Orig Articles Series
1978;14:37-54
33. Scott Chudnoff. Uterine anomalies. Fertil Steril 2002; 78:899·915
34. Simon C, Martinez L, Pardo F, et al. Mullerian defects in women with normal reproductive outcome. Fertil Steril. Dec
1991;56(6):1192-3.
35. Stassart JP. Nagel TC, Prem KA, Phipps WR. Uterus didelphys, obstructed hemivagina, and ipsi\ateral renal agenesis: the
University of Minnesota experience. Fertil Steril. Apr 1992;57(4):756-61.
36. Strassmann EO. Fertility and unification of double uterus. Fertil Steril. Mar-Apr 1966;17(2):165-76
I :
37. Tanaka YO,Kurosaki Y,Kobayashi T, Eguchi N, Mori K, Satoh Y.Uterus didelphys associated with obstructed hemivagina and • .
ipsilateral renal agenesis: MR findings in seven cases. Abdom Imaging. Jul-Aug 1998;23(4):437•41.
38. The American Fertility Society classifications of adnexal adhesions, distal tubal occlusion secondary to tubal ligation, tubal
pregnancies, Miillerian anomalies and intrauterine adhesions. Fertil Steril 1988;49:944
39. Tridenti G, Bruni V, Ghirardini G. Double uterus with a blind hemivagina and ipsilateral renal agenesis: clinical variants in
three adolescent women: case report and literature review. Adolesc Pediatr Gynecol. 1995;8:201.
40. Valle RF.Sciarra Jj. Hysteroscopic treatment of the septate uterus. Obstet Gynecol. Feb 1986;67(2):253-7.
41. Williams EA, Congenital absence of the vagina - a simple operation for its relief. I Obstet Gyneco\ Br Commonw. Aug 1964;
71:511-2.
42. Zanetti E, Ferrari LR, Rossi G. Classification and radiographic features of uterine malformations: hysterosalpingographic
study. Br J Radio!. Mar 1978;51(603):161-70.

391
PEDIATRIC
AND
ADOLESCENT
GYNECOLOGY
■
 SECTION ONE
OVERVIEW OF PEDIATRIC/ADOLESCENT GYNECOLOGY
REPRODUCTIVE TRACT OF CHILDREN & ADOLESCENTS
• The reproductive tract in children and adolescents differ from that of adult females
• Physicians must be aware of the differences, so that the approach is accurate and appropriate

Illustration
vr: Vt
• Responds to
:~
• Genital organs
1.0
cm

• External • Internal/external
cm

OS
cm

placentally receive little genitalia show genitalia take

Physiology
acquired maternal estrogen signs of estrogen on the adult
hormones stimulation stimulation appearance

Uterine/
• 0.25-0.5 • 0.5-1.0 • 1.0-1.5 • 1.5-2.0
cervix ratio*
Labia • Approaches adult
• Bulbous • Flatter • Denser
majora appearance
• Extremely thin
Labia • Thick& • Appear as an • Become • Considerable
minora protruding extension of rounded variation
clitoral hood
• Large but has a • Clitoris begins • Approaches adult
• Less
Clitoris normal index** of to increase in size: width <l cm
prominent
0.6 cm' or less size & length 1.5-2.0 cm

• Initially turgid • Crescent shaped

• Thinner
Hymen and purple-red • Thicker • May be annular or
• Translucent
• Thick & elastic ring-like

• Flushed to the vaginal vault • Becomes

• Flushed to the
Cervix • Not easily palpable separated from
vaginal vault
• Opening only appear as slit the vaginal vault
• Estrogenizedat birth

■
• As estrogen
declines, .
endometrial • Corpus becomes
• Regresses in • Starts to
Uterus lining sheds twice as large as
size enlarge in size
• Vaginal bleeding the cervix
occurs which
stops within 7-10
days after birth

• Descendin true pelvis

• Contain a number of follicles but
• Follicles and cysts • Start of follicular
Ovaries fewer & smaller compared to after
are common development
menarche
• Estrogen increases

• Uterus/cervixratio is defined as the ratio of the length of the uterine corpus to the length of the cervix.The uterus
increases in size with hormonalstimulation.
"The clitoralindex refers to the productof the sagittal and transverse diameters of the glans of the clitoris.
Source: BeiberEJ. Physiologyof the uterus and cervix.Online
395
PUBERTY
• Process by which a sexually immature individual becomes capable of reproduction
• Encompasses a series of neuroendocrine and physiologic changes largely as the result
of the maturation of the hypothalamic-pituitary-ovarian axis, which result in the
ability to ovulate and menstruate
• As a rule, breast development, cornification of the vaginal mucosa, and the growth of
genital hair precede menstruation by 2 years

I. CHANGESIN PUBERTY
• Overview of changes include:
o Development of secondary sex characteristics
o Growth spurt
o Achievement of fertility
• Ratio of fat to both total body weight (TBW) and lean body weight (BW) is the most
relevant factor for onset of puberty and menstruation (obese women have earlier
onset of menarche)

II. SEQUENCEOF PREPUBERTALCHANGES

• Endocrinologic events with onset of puberty:
o Initial: episodic pulses ofLH during sleep
o Last: activation of positive gonadotropin response to increasing levels of estradiol (E2)
• As the HPO-axis matures, hormonal influence on responsive tissues become apparent
during puberty.
• Leptin is the hormone produced by adipocytes which affects LH pulsatility that
results in menstrual cycles (the higher the amount of body fat, the earlier the
menarche)

AGE*
EVENT
I (in years)
• 6-8 years
I HORMONE
• Increase in adrenal androgen production • Peaks
Adrenarche • DHEA-S
derived from the zona reticularis between
13-15
• Activation of the HPO axis
• Involves pulsatile GnRH secretion
stimulating the anterior pituitary to • GnRH
Gonadarche • 9-10 years
release FSH & LH, which trigger the • FSH, LH
ovary to produce estrogens and effect
cyclical ovulation
• First sign of puberty
Thelarche • 10-11 years • Estradiol
• Breast development
• Appearance of axillary/pubic hairs-and
Pubarche • 10-12 years • Androgens
development of the pilo~ebaceous unit
• GH
• Substantial portion of adult height, about
Maximal • IGF-1
17-18% is gained during puberty
growth • 11-12 years • TSH
• Peak height velocity is attained 6 months
velocity • Sex
before menarche
steroids
• First menstruation
Menarche • Last sign of puberty (usually occurs 2-3 • 11.5-13 years • Estradiol
years after thelarche
•Averageage and age range forthe onset of the majorphysicalchanges associatedwithpuberty
DHEA-S:dihydroepiandrostenedione sulfate
GH:growthhonmone
IGF-1:insulin-like
growthfactor-1

396
GYNECOLOGIC EXAMINATION
I. POSITIONS USED TO EXAMINE THE PEDIATRIC PATIENT
POSITION I REMARKS

• Most common
Frog-leg • Child has direct view of examiner
and herself

• For anxious children

Modified • Child between parent's legs and
frog-leg holds child's legs in lithotomy
position

• For older children

• Allows visualization of lower and
upper vagina
• Best for examining child with
Knee-chest
discharge or foreign body

~
• Lateral and downward traction of
the labia improves visualization
into the vaginal canal

~
Sources:SantillanesG, et al. Harwood-Nuss'clinicalpracticeof emergencymedicine,6th edition
ZinnsL, et al. Vaginalbleeding.Online

II. EXAMINATION OF THE EXTERNAL GENITALIA

• Vaginal examination under general anesthesia is the mainstay of evaluation to exclude the
presence of tumors, foreign bodies, or other local causes of bleeding ■

I NEWBORN
I PREPUBERTAL
• Epithelium: uncornified, redder, thinner
• 4-6 cm long
• Labia majora: puffy
• Labia majora: lose fullness
• Labia minora: thickened
Vulva • Labia minora: become thinner and do not fully
• Redundant hymenal folds
and cover the vaginal vestibule
• Mucosa: pink & moist
vagina • Perineum & perivaginal tissues: rigid/inelastic
• Vaginal pH: acidic
• Vaginal pH: is neutral or slightly alkaline
• Discharge: mucoid
• lntroitus: more anterior
• Often crescent-shaped
• Hymen is redundant
• May protrude upon straining
Hymen • Estrogenized
( until 10 years old)
(thick & elastic)
• Clitoris: 1-2 cm (prominent)
397
III. EXAMINATIONOF BREAST DEVELOPMENTAND BODY HAIR DISTRIBUTION
• Stages of development of secondary sexual features in females has been described by
Marshall and Tanner as follows:

STAGE I ILLUSTRATION I BREAST I PUBIC HAIR

I
DEVELOPMENT GROWTH

I r:-,v~
A· ·1' I U/
K~
• Papillae
elevated
(preadolescent)
• No breast
buds
• None

?url ~
• Breast buds • Sparse,

II f!v~
Ao of_ I
and papillae
slightly
elevated
straight,
slightly
pigmented

A'~~1'I ~U!
r!il~ 1~
• Breast
• Darker,
and areola
III confluent,
coarser,
curly
V elevated

• Areola and

IV
t\fj r >ur
i~ papillae
projected
above breast
• Adult-type
pubis

~~/ )U!i~
ffv~ • Papillae • Lateral
V projected distribution

Source:Lobo,et al. Comprehensive

Gynecology.
7thed. 2017

398
 SECTION TWO
DISORDERS OF SEXUAL MATURATON

ADVANCED SEXUAL MATURATION (PRECOCIOUS PUBERTY)

• Sexual precocity is the premature onset of sexual maturation:
o At any age that is 2.5 standard deviation (SD) earlier than the normal, OR
o Appearance of any secondary sexual characteristics before 8 years of age

I. ETIOPATHOGENESIS
• Precocious or advanced sexual maturation is due to:
o An abnormally early hypothalamic-pituitary-ovarian (HPO) activity; or
o Stimulation by estrogens of exogenous or endogenous origins

I GnRH-DEPENDENT
I GnRH- INDEPENDENT
• Production of sex hormones at
• Activation of HPO axis high levels (without activation
Pathology of the HPO axis)
• Central or true precocious puberty • Peripheral precocious puberty

• Early maturation & activation of • Early sexual development from

HPO axis
• Characterized by both breast &
Description pubic hair development
• Early developing sexual
characteristics are isosexual
(consistent with gender)
exposure to sex steroid hormones
that derive from gonads, adrenals,
or environment
• May be isosexual or
contrasexual (inconsistent with
gender)

• Functional ovarian tumor (e.g.,

granulosa cell tumor)
• Idiopathic
• Adrenal tumor
Etiology • CNS lesion
• McCune-Albright syndrome
• Hypothyroidism
• Iatrogenic (e.g., oral
contraceptive pills)
~

'Labor:atory'Rindings "'
FSH, LH l
i
Estradiol (EZ) i
i
Testosterone i i

■
DHEAS
i i .
GnRH response Pubertal Flat

399
II. SPECIFICETIOLOGIES
ETIOLOGY I PATHOGENESIS I FEATURES

GnRH-Depeni!entll
• Seen nearing age of menarche
• No abnormalities except early
development of the secondary
sexual characteristics which
progress in an orderly
• Due to early maturation and
sequence
Idiopathic activation of the HPO axis
• Future menstrual pattern and
(80%) • Random LH > 0.3 lU/L
fertility are expected to be
normal
• May have decreased adult
height due to an accelerated
bone maturation and early
closure of the epiphyses
• Lesions at hypothalamus near the
3rd ventricle, tuber cinereum, or
mamillary bodies • Early sexual development may
CNSLesions • Associated CNS diseases include be due to an early activation of
TB, encephalitis, trauma, the HPO axis
hamartomas, craniopharyngioma,
hydrocephaly
• Primary thyroid insufficiency (e.g.,
Hashimoto thyroiditis ), leads to
• Girls aged 6 and 8 years
increase TSH and gonadotropins
• Precocious puberty is a rare
or Van Wyk-Grumbach syndrome
complication of prolonged
Primary • Exact mechanism is unknown
primary hypothyroidism
hypothyroidism (low thyroid hormone levels may
• Bone age is retarded: unique to
lead to compensatory production
hypothyroidism
ofTRH which may cross react with
GnRH in the pituitary because
they share the same alpha-subunit

GnRH-lndepende4f" ~ "'' •
• Tumors of the ovary that produce
estrogen or stimulate estrogen
production: granulosa cell tumor
(most common), thecoma,
• Estrogen-secreting tumors can
luteoma, teratoma, follicular cyst
Sex steroid cause breast development and
• Tumors of the ovary that produce
producing vaginal bleeding
tumors androgens: Sertoli-Leydig tumors
• Androgen-secreting tumors can
• Extragonadal tumors may also be
cause virilizing features
hormonally functional and able to
produce or induce the production
of sex hormones (e.g., adrenal
adenomas and hepatomas)
• May have feminizing
(isosexual) or virilizing
• Both adrenal tumors and
(contrasexual) effects
late onset congenital adrenal
• If treated during neonatal
hyperplasia can cause virilization
Adrenocortical period, normal puberty ensues.
• Diagnosed using adrenal imaging,
• If treated late, feminizing
21- or llB-OHase or 3B-ol
features appear.
dehydrogenase
• If untreated, develops virilizing
features
400
 ETIOLOGY
I PATHOGENESIS
I FEATURES
• Vaginal bleeding (first sign)
• Mutation in G3 protein activating • Complex genetic disorder
adenylate cyclase affecting the bone, skin and
McCune • Constant stimulation of FSH, LH, endocrine systems
Albright TSH & GH • It is characterized by:
syndrome • The prognosis is unfavorable: precocious puberty,
most patients have menstrual polyosthotic fibrous dysplasia,
abnormalities and are infertile and irregular cutaneous
pigmentation (cafe-au-lait spots)

• Possible although uncommon

cause of early feminization
• Can be due to prolonged intake of
hormonal pills or application of
estrogen creams • Early breast maturation has
Iatrogenic or
• Chemicals in the environment been shown to be caused by
factitious
with endocrine disrupting EDCs
chemicals which may
have estrogen-like actions
( examples: phthalates,
dichlorodiphenyldichloroethylene)
Source:Philippine
Societyof Reproductive
Endocrinology
andInfertility,
2012

III. MANIFESTATIONS
• History: Life threatening causes like neoplasms of ovary, adrenal or CNS
• Physical exam: Premature appearance of secondary sexual characteristics
• Early growth spurt with resultant shorter adult height
• In GnRH-dependent precocious puberty, the bone growth is also advanced for age
• Exception: primary hypothyroidism ( only cause of GnRH dependent precocious puberty
where bone age is retarded)
GnRH-
GnRH Dependent Syndromes* lndependent
Syndromes*
FINDINGS
McCune
Idiopathic CNS Tumors Hypothyroidism Albright
Syndrome
Breast
Yes Yes Yes Yes
enlargement
Pubic hair Yes Yes Unusual Yes
Vaginal

■
bleeding
Yes Yes Yes Yes
.
"rili i g s·g s No No No No
Bone age Advanced Advanced Normal or retarded Advanced
Neurologic
No Yes No Yes
deficits
Abdominopelvic Occasional
findings Occasional bloating,
No No
masses constipation,
and/or ascites
·In GnRHdependentprecociouspuberty,physicalchangesare typically
thoseof normalpuberty,withthe exceptionof the
"ageof onser. InGnRH-independent
syndromes,physicalchangesare markedlydiscordantfromnormalpuberty

Source:Loboet al.,Comprehensive
Gynecology,
7th Edition,2016.

401
IV. DIAGNOSIS
A. Indications for Evaluation of Precocious Puberty:
o <6 years of age with breasts OR pubic hair
o <8 years of age with breasts AND pubic hair
o <8 years of age with breasts OR pubic hair (warrant careful history and PE, bone
age, and close follow-up to determine linear growth rate)
o Those with increased risk for intracranial pathology (onset of puberty <6 years old,
rapid pubertal progression, symptoms of headache, seizures, or neurologic deficits)

B. GnRH Agonist Stimulation Test

o Considered when initial tests are inconclusive
o Procedure: leuprolide acetate is given, then estradiol is measured
o Differentiates "true (GnRH-dependent)" from "pseudoprecocious"
(GnRH-independent) puberty
, GnRH-dependent: gonadotropin responses are pubertal (true precocious puberty)
, GnRH-independent: gonadotropin responses are prepubertal (pseudoprecocious
puberty)

C. Other Diagnostics
o Brain imaging, EEG's
o Ultrasound, CT or MRI of abdomen
o Serum FSH, LH,TSH, PRL, E2, testosterone, DHEA-S,hCG, androstenedione, 17-OH
progesterone, T3 and T4
o Genetic testing

V. MANAGEMENT
• Reduce gonadotropin secretions
• Reduce or counteract the peripheral actions of sex steroids
Goals of therapy
• Reduce the growth rate to normal
• Slow down skeletal maturation to allow maximal adult height
• Indications for medical therapy:
0 Menarche <8 years old
0 Progressive thelarche & pubarche
0 Bone age >2 years of chronological age
• Depending on etiology
Medical therapy
0 GnRH dependent: GnRH agonist (leuprolide - drug of choice,
goserelin, triptorelin)
0 GnRH independent: estrogen antagonist therapy (e.g., aromatase
inhibitors - letrozole or anastrazole) or estrogen receptor
antagonist (e.g., fulvestrant)
Surgical therapy • Removal of tumor or lesion producing excess hormones

402
VI. INCOMPLETESEXUAL PRECOCITY
• Occasionally due to unknown reasons, only one sign of pubertal development will be
individually present (breast development, pubic hair growth, or menstruation).
• This is possibly the result of:
o Transient elevation of circulating steroid hormones
o Extreme sensitivity of the end organs to the low prepubertal levels of sex hormones
o Variant of normal puberty
• Usually self-limiting (treat or remove underlying cause, if any)

ETIOLOGY/
DISORDER
I FEATURES
I MECHANISMS
• Isolated development of the breast prior to
the age of 8 years
0 Breast buds enlarge (often asymmetric)
0 Nipple development is absent
• Transient ovarian
0 No axillary or pubic hair development
follicular activity
0 Somatic growth pattern is not
Premature • Exogenous source
Thelarche accelerated
(e.g., environment or
0 Normal linear growth & bone age, adult
height is not affected diet)
0 Smears of the vagina fails to show estrogen
effect
0 Benign, self-limiting; biopsy of the breast
tissues is unnecessary
• Isolated development of pubic hair before
• These may be signs
the age of 8 years without other signs of
of excess androgen
precocity
0 Non-progressive, no clitoral hypertrophy
production due to:
Premature 0 Some with abnormal EEGwithout neuro
0 Enzymatic
Pubarche deficiency
disease
(congenital adrenal
0 Bone age not advanced, adult height is not
hyperplasia)
affected
0 Tumors (Leydig
o -Increased androgen (DHEA & DHEA-S)by
cell tumor)
adrenal glands
• Isolated development of axillary hair before
the age of8 years without other signs of
precocity • May evolve into
Premature
0 Bone age not advanced, adult height is polycystic ovary
Adrenarche
not affected syndrome
0 Increased androgen (testosterone and
17-0H progesterone)
• Denotes the occurrence of cyclic vaginal

■
bleeding in prepubertal girls without other
Premature.,,, sighs of secondary sexual development • Cause is unknown,
Menarche
0 Bon(!age not advanced, adult height is not
idiopathic
affected
0 Resultant menstrual pattern is normal
0 Fertility potential is ~nimpaired

403
DELAYED SEXUAL MATURATION
• Defined as the absence of normal pubertal changes at an age 2.5 SD from the mean
• The absence of thelarche by age 14 or of menarche by age 16 is an indication for investigation

I. HYPOGONADISM

Cause of Lack
I HYPERGONADOTROPIC
HYPOGONADISM*
• Due to primary ovarian failure (two
I HYPOGONADOTROPIC
HYPOGONADISM
• Due to the lack of pubertal
of Gonadal intact X chromosomes are needed maturation of the hypothalamus
Function for normal ovarian function) and pituitary
Gonadotropin
• Elevated • Low
Levels
• Hypoestrogenism
Manifestations • Undeveloped breasts and little or no pubic hair
• Atrophied cells on smear of the vaginal walls
• Turner syndrome: gonadal
dysgenesis due to X chromosome • Reversible causes:
deletion (See Section 3) 0 Weight loss/fat loss
• Ovarian failure with normal sex 0 Marked protein deficiency
chromosomes (46XX)due to: 0 Cranial tumors (e.g., pituitary
Examples
0 Mumps adenoma, craniopharyngioma)
0 Infiltrative disease • Irreversible causes:
(e.g., TB of ovary) 0 GnRH deficiency
0 Autoimmune diseases 0 Hypopituitarism
0 Environmental agents

• For constitutional hypgonadotrophic

hypogonadism: reassurance
• LH-releasing hormone challenge
test differentiates constitutional
• Hormone replacement therapy
Management delays with other conditions
given in a cyclic manner
associated with a deficiency of
gonadotrophin-releasing factors
• For tumors: shrink or removal,
when feasible
'The largestnumberof patientswithdelayedsexualdevelopmenthave hypergonadotrophic
hypogonadism

II. EUGONADISM
• Estrogen levels are sufficient with timely appearance of secondary sexual characteristics.
• Most have well-formed female body configuration with developing breasts.
• Menarche does not occur because of absent ductal elements or obstruction of the
menstrual outflow tract
• Congenital anomalies of the paramesonephric (Mullerian] structures:
o Responsible for most eugonadal patients with amenorrhea or cryptomenorrhea
o Most frequent defect is the absence of the uterus and vagina
• Other causes: imperforate hymen, transverse vaginal septum, agenesis/atresia of vagina
• For obstructive causes, corrective surgery is indicated

Ill. VIRILISM
• Virilization may delay development of normal secondary sexual characteristics in girls:
o Small breasts
o None or irregular menstrual cycles
• Masculinization may be manifested by all or a combination of the following:
o Enlarged clitoris
o Acne formation
o Deepening of voice
o Excessive facial hair and male-pattern baldness
• Virilization at puberty is the result of elevated androgens from adrenal or gonadal
sources (may be the result of an enzyme deficiency as in late-onset congenital adrenal
hyperplasia or neoplasm as in Sertoli-Leydig cell tumor]
• Management is the removal or treatment of underlying cause
404
 SECTION THREE
DISORDERS OF SEXUAL DEVELOPMENT (DSD)

ERRORS IN SEXUAL DETERMINATION

• Disorders of sexual differentiation result when errors occur at any of the steps involved in
the genetic, embryologic, & physiologic development of a fetus along male or female lines

TERM
I DEFINITION
Genetic or • Defined by the sex chromosome, typically XXor XY
chromosomal sex
• Defined by the direction of gonadal differentiation into ovaries or
Gonadal sex
testes, as directed by genetic sex
• Defined by the appearance of external genitalia and the secondary
Phenotypic sex sexual characteristics that develop at puberty as controlled by the
hormonal environment directed by gonadal sex

I. 46, XX DISORDERS OF SEXUAL DEVELOPMENT (VIRILIZED FEMALES)

• Maybe secondary to disorders of gonadal development, androgen excess, or other
disorders of genital development

ETIOLOGY
I PATHOGENESIS
I FEATURES

Ovotesticqlar Diso1'de1'-o[Sexual J!evelopment (Hermaphroditism)

• 70% are • Translocation of testis • True hermaphrodites born with
46XX, the rest determining genes from the Y to both ovarian and testicular
are 46XY or the X chromosome tissues (may include bilateral
4SXO,46XY • Autosomal dominant mutation ovotestis and a contralateral
mosaic that promote testes development ovary or testis)
in the absence of a Y chromosome • Extent of development of
the embryonic Wolffian
ducts depend on activity of
the Leydig cells, while the
Mullerian will depend on the
Sertoli cells of the testicular
portions of the gonads
- 1
Congtnital Ad-,,enal.'Hyperplasia (Adrenogenital Syndrome)
• Virilization of • Due to adrenal androgen • Female pseudohermaphrodites:
a 46XX fetus overproduction in the fetus female genotype, varying

resulting from a defective cortisol
and aldosterone biosynthesis
brought about by an enzyme
deficit (usually 21-hydroxylase
deficiency)
Mu[lerian Agenei1s(or ~ayer-Rolflta_nsk~-Kuste~ Hauster Synclr-;,,rie)
• Due to • Failure of the uterus and the
chromosomal vagina to develop properly in
translocations women who have normal ovarian
function and normal external
genitalia
■
degrees of virilization .
• Genital ambiguity: clitoral
enlargement, labial fusion and
abnormalities of the urethra
and the vagina
• Primary amenorrhea,
normal breast and pubic hair
development, and no vaginal
canal

405
II. 46XY DISORDERSOFSEXUALDEVELOPMENT(INCOMPLETELY MASCULINIZED MALES)
• May be secondary to disorders of testicular development, disorders of androgen
synthesis, disorders of androgen action, LH receptor defects, or disorders of AMH and
its receptors

• X-linked or • Deficiency of both • Generally present after the expected

autosomal Leydig and Sertoli Cell time of puberty with delayed sexual
dominant trait development maturation, primary amenorrhea,
expressed only normal pubic hair, and normal female
in genotypic internal and external genital anatomy
males • Lack of testicular androgen results in
female external genitalia
• Lack of Mullerian Inhibiting Factor (MIF)
results in the persistence of the Mullerian
ducts (uterus and fallopian tubes)
• Lack of estrogen from the streak gonads
leads to amenorrhea and absence of
female secondary characteristics
Androg vtty$yndro~e fII on) or
Male P hrodite
• Male genotype • Genetic males whose • Testes are undescended and maybe
(46XY), female target cells lack found in the abdomen or more
phenotype receptors for androgens frequently, the inguinal canal
(with some (absence of penile • Feminized due to lack of inhibitory
degree development and influence of testosterone on estrogen's
of breast undescended testes) effects on responsive tissues (like the
development breast)
and female • Have normal testes that produce normal
external amounts of MIF; hence, there is no
genitalia) development of Mullerian structures
(uterus, fallopian tubes, cervix)

406
III. SEX CHROMOSOME DISORDERS OF SEXUAL DEVELOPMENT
• Results from defective gametogenesis, often non-disjunction
• Chromosomes fail to separate (non-disjunction) therefore both go to one of the daughter
cells during meiosis, the other has none

ETlOPATHOGENESlS
I FEATURES

1, Turner Syndrome - -- --
• Complete absence of one • Commonly presents with short stature, absence of
sex chromosome: leads to sexual development, a webbed neck, low set ears
monosomy X (45XO) genotype and posterior hairline, widely spaced nipples (shield
chest), short fourth metacarpals, and cubitus valgus
• May have renal, cardiac, and ocular anomalies
• Presents at adolescence with primary amenorrhea
and absence of pubertal development
Klinefelter5yndrome
--- ,, X

• Results from meiotic
nondisjunction that leads to a
47XXYgenotype
• Most common congenital cause
ofhypogonadism in males
Mixid (:onadal Dysgenesis
• 45XO/ 46XY is the most
commonly associated
karyotype
• Phenotype in MGDcan vary
widely, reflecting the relative
proportions of 45XO and 46XY
in the gonadal ridge
• Habitus exhibits long arms and legs, due to both
a long bone abnormality and the influene of
testosterone deficiency, and a short trunk
• Presents with testicular atrophy, gynecomastia, and
female hair distribution
• Asymmetrical gonadal dysgenesis, where one gonad
can be identified as a testis and the other is a streak
gonad or absent altogether
• Genitalia are typically ambiguous, but can also be
female or male
• Incidence of gonadal tumors is relatively high (25%)

APPROACH TO MANAGEMENT

• Karyotyping
Diagnostic
• Other tests to support diagnosis and management of specific
work-up
causes (e.g., ultrasound, enzyme assays)
• Individuals with DSDs should be allowed to develop a gender
Gender
identity for him or herself with the help of the parents and the
assignment
guidance of a child and adolescent psychologist

■
Hormonal&
• Applicable hormonal replacement may be given to achieve the .
desired secondary sexual characteristics
other medical
• Medical treatment of associated co-morbidities should be given as
treatment
indicated
1,, • Removal of the gonads is performed on a phenotypic female with a
Y chromosome as prophylaxis against gonadoblastoma before age
Surger;y 19 years of age
• Gender assignment surgeries are put off until the individual with
DSD is of legal age to decide for themselves
Assisted • Often infertile or even sterile, reproductive efforts sometimes
reproductive
involve third-party ART* (e.g., ovum and/or sperm donation,
techniques
surrogacy, etc.)
(ART)
'Not practicedinthe localsetting

407
 SECTION FOUR
MENSTRUAL DISORDERS
ABNORMAL UTERINE BLEEDING (AUB)
• Vaginal bleeding is one of the most common problems in the adolescent female

I. ETIOPATHOGENESIS& MANIFESTATIONS
• Physiologic immaturity of the HPO feedback mechanism
• Blunting of the LH surge resulting in anovulation
• Excessive endometrial stimulation by estrogen
• Absence of the formation of the corpus luteum that brings about an inadequate
production and withdrawal of progesterone
• Excessive proliferation of the endometrium and non-uniform sloughing in different
areas of the endometrial lining.

II. MANAGEMENT
• Observation and reassurance
Minimal
• May resolve in time by itself with the maturation of the HPO axis
bleeding
• Iron supplementation
• Acute bleeding
• Hospitalization may be needed to administer of high doses of
estrogen to facilitate re-epithelialization of the endometrial lining
over the denuded areas
Severe 0 Once bleeding stops, progesterone is added to stabilize the
bleeding endometrium and to ensure uniform sloughing upon withdrawal
° Fibrinolytics and hematinics may be given
• Chronic bleeding: cyclic regulation of the menses for the next 3-6
months may be achieved by giving cyclic progesterone or combined
contraceptive pills, after which a period of observation follows

PRIMARY DYSMENORRHEA
I. ETIOPATHOGENESIS
• Development of painful menstruation in the absence of an organic cause
• Prostaglandin theory: most accepted theory to explain occurrence of dysmenorrhea
• Prostaglandins released during menstruation induces uterine muscle and vascular
contraction that causes uterine contractions and ischemia respectively

II. MANIFESTATIONS
• Tightness of the internal os has been implicated with the observation that symptom
improves with menstrual egress

III. MANAGEMENT
• Primarily directed towards reassuring the patient and the mother that such condition
will disappear or resolve with time
• Menstrual cramps may be alleviated by giving analgesics with prostaglandin
synthetase inhibiting properties (e.g., NSAIDS)

408
 SECTION FIVE
OTHER 01SORDERS IN PEDIATRIC GYNECOLOGY
VULVOVAGINITIS
I. ETIOPATHOGENESIS
• Most common gynecologic disorder/complaint in children
• The child is susceptible to this kind of infection because of the following reasons:
o Lack of estrogen (which makes the vaginal mucosa thin and atrophic)
o Possibly immature immune mechanisms in the vagina
o Contamination by stool and other debris (poor perinea! hygiene)
• Organisms: group A or B beta-hemolytic streptococcus, H.injluenzae, Enterobius vermicularis

II. MANIFESTATIONS
• Area of redness/soreness limited to perineum or may extend to thighs and/or anus
• Acute vulvovaginitis may:
o Denude the thin vulvar and vaginal mucosa
o Have varying vaginal discharge from scant to copious
o Have bleeding, but usually minimal
• The irritating discharge often causes the child to scratch the area to the point of bleeding.

Ill. DIAGNOSIS
CLASSIFICATION I REMARKS

• Involve an irritation of the vulvar epithelium by normal rectal flora or

Non-specific
chemical irritants
vulvovaginitis
• Secondary to poor hygiene or foreign body
Secondary • Infection from pathogens affecting other areas of the body
Inoculation • Contamination by direct contact or blood born transmission (URTI,UTI)
Specific • Primary infection
vulvovaginitis • May be sexually transmitted (e.g.,N. Gonorrea,G.Vagina/is,T.Pal/idum,HSV)

IV. MANAGEMENT
• Lifestyle modification:
o Good perinea! hygiene (front-to-back wiping) and avoid harsh soaps
o Frequent change of cotton underwear to absorb discharge
o Wear loose fitting clothes
o Urination with legs spread apart to separate the labia
• Infection: broad spectrum antibiotics (e.g., amoxicillin), antivirals, or antihelminthics
as indicated
• Pruritus: antihistamines or low potency topical corticosteroids for the pruritus
• In recurrent infections refractory to treatment or associated with a foul-smelling,
bloody discharge, it is necessary to exclude foreign body or tumor

.;;;.U..;_R=E;.,;;.T..;_H"'"RA"-=L;...;;P....;;R..;;,.O;;_L=A-"P;_S=E=--------------------1
I. ETIOPATHOGENESIS
• Urethral mucosa protrudes through the urethral meatus which forms a hemorrhagic,
sensitive vulvar mass due to lack of estrogen

II. MANIFESTATIONS
• Prepubertal bleeding (most common symptom)
• Red mucosa! circumferential mass prolapses out of the urethral opening after coughing

III. MANAGEMENT
• Small lesion without impairment of urination: expectant management, often resolves in time
• Small lesion with mild impairment of urination: short course of daily topical application
of estrogen cream
• Large and necrotic lesion with or without urinary retention: resection of the prolapsed
tissue and submit tissue for biopsy to rule out malignancy; insertion of indwelling catheter
409
FOREIGN BODIES
I. ETIOPATHOGENESIS
• Foreign bodies in the vaginal canal induce an intense inflammatory reaction and
result in blood-stained, foul-smelling discharge

II. MANIFESTATIONS
• Foul-smelling, bloody vaginal discharge (classic symptom)
• Partially buried or embedded object in vagina
• Examine child in the knee-chest position to better visualize foreign objects within the
vaginal canal

III. DIAGNOSIS
• Not always a reliable imaging technique to visualize foreign
Radiographs
objects within the vagina, since most objects are not radioopaque
Vaginoscopy • To identify and remove obje~ and exclude other causes of bleeding

IV. MANAGEMENT
• Proper care and hygienic instructions to the mother and child are indicated
• Management consists mainly of the removal of the foreign material:

Foreign bodies in • Can be removed with the bayonet forceps

the lower third of • Preferably flushed out with a warm saline irrigation on direct
the vagina visualization
Foreign bodies deep
• May have to be removed with vaginoscopy under general anesthesia
in the vaginal canal

LABIAL ADHESION
• Fusion of the labia minora at the midline (i.e., the two labia minora are "stuck" together)
• Pathognomonic sign is the presence of a mid line vertical line in between the labia minora

I. ETIOPATHOGENESIS
• Common in prepubertal girls
• Due to irritation/inflammation of "unestrogenized" epithelium with adhesions
forming during the healing process
• Related to low levels of estrogen
o Skin covering the labia is extremely thin, and local irritation induces scratching,
which may denude the labia
o Labia minora then adhere in the midline and stick to each other in the process of healing
o Re-epithelialization occurs with the labia minora remaining fused to each other

II. MANIFESTATIONS
• Asymptomatic: incomplete labial adhesions
• Important to differentiate this condition from congenital absence of the vagina
• Symptoms are usually related to obstruction in urine flow or accumulation of urine
behind the filmy adhesion
• Cardinal symptoms: dysuria, and recurrent vulvar & vaginal infections
• Recurrence is common until puberty because of low estrogen

III. MANAGEMENT
Asymptomatic to
• Need not be treated
minimal/moderate
labial fusion
• Often separate naturally in time

·•Estrogen cream applied twice daily for 7-10 days or until the
Symptomatic fusion is released spontaneously
labial fusion • For tenacious adhesions: simple midline incision along the fusion
,, line l:o separate the labia minora
410
LICHEN SCLEROSUS
I. ETIOPATHOGENESJS
• Hypotrophic dystrophy of the vulva
• Most common in prepubertal & postmenopausal age groups
• Histologically, the findings are:
o Flattening of the rete pegs
o Hyalinization of the subdermal tissues
o Keratinization

II. MANIFESTATIONS
• Presents with flat ivory papules that may coalesce into plaques that, in extreme cases,
involve the entire vulva
• Usually, does not extend laterally beyond labia majora nor does it encroach into vagina
• Clitoris is frequently involved as well as the posterior fourchette and anorectal area
• Symptoms consist ofvulvar irritation, dysuria and pruritus.
• Scratching is common leading to an increased tendency to bruising, formation of
bloody blisters, and secondary infections

Ill. DIAGNOSIS
• No known malignant potential if only hypoplastic dystrophy is present
• Histologic confirmation may be necessary in postmenopausal women, but not always
indicated in children
• Resolution of the condition with a clinical trial of daily application with estrogen
cream eliminates the need for a biopsy
• If the lesion appears to be lichen sclerosus to the experienced observer, histologic
confirmation is usually not necessary

JV.MANAGEMENT
• Topical estrogen
• Hydrocortisone cream
• Improved perinea) hygiene

VAGINAL BLEEDING
• Vaginal bleeding at any time may be due to trauma or tumors
• Differentials for bleeding, depending on the onset of menarche is summarized below:

·.
BLEEDING BEFORE MENARCHE I BLEEDING AFTER MENARCHE

• Hormonal-related: • Bleeding tendencies

o Neonatal bleeding • Infection
o Exogenous estrogen • Endocrinologic pathologies: ■.;
o Precocious puberty o Midcycle spotting
• Non-hormonal-related: o Abnormal uterine bleeding (e.g.,
o Urethral prolapse contraception, PCOS,hypothyroidism)
o Genital warts • Ectopic pregnancy
o Lichen sclerosis • Spontaneous abortion
o Infectious vaginitis • Placenta previa
o Foreign body • Abruptio placentae
Source:ZinnsL.Vaginalbleeding.Online

411
 SECTION SIX
GYNECOLOGIC TUMORS

OVERVIEW OF GYNECOLOGIC TUMORS

• Cancer of the female genital tract in children/adolescents is rare, but is associated
with poor prognosis

I. EPIDEMIOLOGY
Although rare, every type of genital neoplasm reported in adults has also been found
in girls under 14years of age
• Benign tumors of the vulva and vagina are rare in childhood, and may seldom cause
bleeding
• Ovarian tumors account for the majority of tumors in pediatric adolescent patients (in
contrast to adults)

II. MANIFESTATIONSAND DIAGNOSIS

• Malignant neoplasms usually bleed from necrotic or ulcerative areas that appear early
in development
• About half the genital tumors in children are premalignant or malignant
• All suspicious lesions require biopsy for diagnosis

TUMORS OF THE VULVA, VAGINA, AND CERVIX

I. BENIGNTUMORS OF THE VULVAAND VAGINA

Unilocular • Encompasses most benign tumors of the vagina in the children

remnants of the • Small cysts of the mesonephric duct do not require surgery when they
mesonephric are asymptomatic.
duct (Gartner • Large cysts must be treated surgically
duct cysts)
• Usually present as cystic masses arising from the midline of perineum
Teratomas • A margin of healthy tissue is excised about the periphery of the mass
to prevent recurrence
Capillary • Usually disappear as the child grows older and thus require no
hemangiomas therapy except for giving reassurance to the mother
• Composed of vessels of considerable size
Cavernous
• Injury to them may cause serious hemorrhage and are best addressed
hemangiomas
surgically

II. MALIGNANTTUMORS OF THE VAGINAAND CERVIX

• Most commonly seen in very young girls(< 3 years old)
• Usually involves the vagina, but the cervix may be affected as well.
Sarcoma • The tumors arise in the submucosal tissues and spread rapidly
Botryoides beneath an intact vaginal epithelium
• Vaginal mucosa then bulges into a series of polypoid growths (thus,
the term botryoid, meaning grape-like)
• Three types of vaginal carcinoma may appear during childhood and
the early teens:
Vaginal 0 Endometrioid carcinoma
Carcinoma 0 Mesonephric carcinoma
0 Clear cell carcinoma
• Features and management are similar to those of adult women

412
TUMORS OF THE OVARIES
I. ETIOPATHOGENESIS
• Ovarian tumors of all varieties (except for Brenner tumors) have been reported in
premenarcheal children, with benign cystic teratoma accounting for at least 30%
• Incidence of malignant degeneration of the neoplasms is higher in children than in the
adolescent or adult women

II. MANIFESTATIONS
• Two most common manifestations: abdominal pain & mass
Symptoms • Hormone-producing ovarian tumors may cause vaginal bleeding
and early appearance of secondary sexual characteristics
• The small pelvic cavity of the child causes most ovarian tumors to
Signs
rise above the pelvic inlet and present abdominally

III. MANAGEMENT
• Management in premenarcheal children varies from that of older patients
• Continued ovarian function is needed to complete sexual & somatic maturation in children
• Fertility sparing surgery is the standard of care

• Oophrocystectomy should be attempted

For benign cases
• At most, an oophorectomy may be done
For stage I ovarian • Unilateral salpingooophorectomy and complete surgical staging is
cancer justified when the tumor is limited only to one ovary
• Germ cell tumors: fertility-sparing surgery may be performed
For tumors that
• Advanced epithelial and sex-cord stromal tumors: more radical
extended beyond
surgery (bilateral salpingooophorectomy, hysterectomy, and tumor
one ovary
debulking) is already indicated

REFERENCES
LBeiber EJ. Physiology of the uterus and cervix. Abdominal key. Available online: https://abdominalkey.com/physiology-of-
the-uterus-and-cervix/#F3-3. Accessed June 23, 2021
2.Lobo RA,GershensonDM, Lent'l GM, Valea FA.Comprehensivegynecology. 7th edition. Elsevier,2016
3.Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice Guidelines on Pediatric and Adolescent
Gynecology.First Edition. November 2012.
4.QuickReferenceManualon ReproductiveEndocrinologyand Infertility; 1st ed., Diliman,QuezonCity: PhilippineSocietyof
ReproductiveEndocrinologyand Infertility,Inc.,2012
S.SantillanesG,Gausche•HillM. Harwood·Nuss'clinical practiceof emergencymedicine.6th edition. Availableonline: https:/ /
doctorlib.info/medical/clinical•practice•emergency•medicine/288.html.AccessedJune23, 2021
6.Taylor HS, Pal Land Seli E (eds.) Speroff's Clinical Gynecologic Endocrinology and Infertility, 9th edition. Philadelphia: ■
Wolters Kluwer; 2020. · "'
7.Zinns L, Chuang J.Posner JC,ParadiseJ.Vaginal bleeding. Anesthesiakey. Available online: https://aneskey.com/vaginal· ~ •
bleeding-4/. Accessed June 23, 2021 ·

413
REPRODUCTIVE
GYNECOLOGY
 SECTION ONE
AMENORRHEA

OVERVIEW OF AMENORRHEA
• The absence of menstrual bleeding is a common gynecologic complaint seen in clinics
• Amenorrhea is a normal feature in prepubertal, pregnant, and postmenopausal females
• In the absence of pregnancy, the exact cause of amenorrhea must be determined
• May be primary or secondary, based on whether patient already had her menarche

I. DEFINITIONOF TERMS
TERM
I GENERAL DEFINITION
• Defined as the absence of menstrual bleeding, which may be
Amenorrhea
primary or secondary
• Condition caused by anatomic disorders interfering with the outflow
Cryptomenorrhea
of menses (e.g.,imperforate hymen, transverse vaginal septum)
Primary Versus Se~ondary Amenorrhea
Primary • Failure of menarche to occur when expected in relation to the
amenorrhea onset of pubertal development
• Cessation of menses for an arbitrary period (usually >6 months)
Secondary
sometime after menarche has occurred
amenorrhea
• Most common cause is pregnancy (should always be ruled out)
Source:GershensonOM,et al. Comprehensive
Gynecology;
2022

II, MAJORCAUSESOF AMENORRHEA

CATEGORY I POSIBLE ETIOLOGIES
• Breastfeeding, pregnancy
Physiologic
• Menopause
• Hormonal contraception, GnRH analogs, antidepressants,
Pharmacologic
chemotherapeutic agents
• Congenital: imperforate hymen, Mullerian agenesis, transverse
Outflow tract
vaginal septum
disorders
• Acquired: Asherman syndrome, cervical stenosis
Primary ovarian • Congenital: gonadal dysgenesis, Turner syndrome
insufficiency • Acquired: autoimmune destruction,, radiation exposure
• Autoimmune disease
• Cushing syndrome

■
• Hyperprolactinemia, prolactinoma
Pituitary
• Infiltrative disorders: sarcoidosis
• Drugs: antidepressants, antihistamines, opiates, cocaine
• Sheehan syndrome, Simmonds syndrome
• Gonadotropin deficiency: Kallmann syndrome
• Infections: meningitis, tuberculosis, syphilis
Hypothalamic
• Metabolic disorders: functional gastrointestinal malabsorption, rapid
weight loss, eating disorder, stress (e.g. competitive physical activity)
• Thyroid disease, polycystic ovary syndrome (PCOS),ovarian tumors
Other endocrine • Constitutional delay of puberty
gland disorder • Adrenal disease, androgen-secreting tumor, adult-onset adrenal
hyperplasia

417
PRIMARY AMENORRHEA
• Failure of menarche to occur when expected in relation to the onset of pubertal development:
• No menarche by age 15, or within 5 years after initial secondary sexual characteristic
development at age 10
• Problem may be endocrinologic or anatomic

Evaluation of Primary Amenorrhea

History and physicalexamination completed

for a patient with primary amenorrhea

Yes
Secondarysexualcharacteristicspresent?

Measure
FSHand LH

FSH<5 IU/L FSH>20 IU/L

LH <5 IU/L LH >40 IU/L

Hypogonadotropic Hypergonadotropic
hypogonadism hypogonadism

46XX 45XO

Premature Turner
ovarian failure syndrome

Do ultrasonography
of the uterus

Uterus absent Uterus present

or abnormal or normal

No Outflow Yes
obstruction

Imperforate
hymen or
transversevaginal
46XY
septum

Evaluatefor
Androgen Mullerian secondary
insensitivity agenesis amenorrhea

The evaluationof primaryamenorrheabeginswith a carefulhistoryand physicalexaminationfollowedby imaging

studiesand hormonaltests. In somecases,karyotypingmay be needed.It is usefulto groupcauseson the basis
of whethersecondarysexualcharacteristics(breasts)and femaleinternalgenitalia(uterus)are presentor absent.

Source:Master-HunterT, et al. Am FamPhysician.2006

GershensonOM,et al. Comprehensive Gynecology;2022
418
General Categories
• The differentials for amenorrhea may be categorized into four groups based on the
presence or absence of breast development and the uterus
WITHOUT BREAST WITH BREAST

t • t •
• 17,20 desmolase deficiency • Androgen resistance
• Agonadism • Uterovaginal agenesis
• 17a-OHase deficiency (46XY)
WITHOUT
UTERUS

d d

CATEGORY! CATEGORY4
• Hypothalamic failure • Hypothalamic/pituitary/
• Pituitary failure ovarian/uterine causes
• Gonadal failure • Outflow tract obstruction
* Treat as secondary amenorrhea
WITH
UTERUS

Quick rules to remember:

If with NO breast and ...

• L FSH:considerhypothalamic or pituitaryin etiology(hypogonadotropic
hypogonadism)
• i FSH:considerovarianetiology(hypergonadotropic hypogonadism)

If NO uterus and ...

• 46XX:considerMullerianagenesis
• 46XY:considerandrogeninsensitivity

419
I. CATEGORY 1: UTERUS PRESENT AND BREASTS ABSENT (Most Common)
• Phenotypically female with absent secondary sexual maturation characterized by
markedly underdeveloped breasts
• Lack of breast development means low estrogen production, check FSH levels to establish
etiology

1. Hypogonadotropic hypogonadism (Low FSH)

Pituitary Gonads

!GnRH
___ _.. , ...;.
USH
__ .,.
!LH 0 , ____. ! Estrogen

• Insufficient GnRH secretion due to neurotransmitter defect

A. Hypothalamic • Inadequate GnRH synthesis (Kallmann syndrome)
failure • Congenital anatomic defect in CNS
• CNS neoplasm (e.g., craniopharyngioma)

Hypothalamus Pituitary Gonads

! FSH
tGnRH
...;.!_L_H
_ _. 0 ____.
! Estrogen

• Isolated gonadotrophin insufficiency

• Pituitary neoplasia
B. Pituitary failure
• Prepubertal hypothyroidism
• Mumps, encephalitis
2. Jiypergonadotropic hypogonadism (High FSH)

Pituitary Gonads

A..
tFSH
_G_n_R_H_.,.~ ....;t_L_H
_ _.. 00 ____.
! Estrogen

• 45X (Turner syndrome): most common

• 46X; Abnormal X (Deletion disorders)
• 46XX: Pure gonadal dysgenesis (Perrault syndrome)
Gonadal failure
• 46XY: Pure gonadal dysgenesis (Swyer syndrome)*
• 46XX: 17-alpha-hydroxylase enzyme deficiency
• Mosaicism (X/XX, X/XX/XXX)
'Exception
totherule:although
46XY,
gonads
areseverely
dysgenetic
thatnoMullerian
Inhibitory
Factor(MIF)isproduced
to prevent
uterine
development

420
II. CATEGORY2: UTERUS ABSENT AND BREASTS PRESENT
• Phenotypically female with absent uterus and variable vaginal length
• Breast development means estrogen is present
• Karyotyping should be done to differentiate the possible causes
° Complete vaginal agenesis (Mayer-Rokitansky-Kiister-Hauser)
0 Androgen insensitivity syndrome (historically, "testicular feminization")

COMPLETE VAGINAL
AGENESIS ANDROGEN INSENSITIVITY
(Mayer-Rokitansky-Kuster- SYNDROME
I Hauser Syndrome) I
• Lack of androgen receptors
• Vaginal agenesis and no uterus
in target organs: no
Pathophysiology • Second most common cause of
differentiation of male external
primary amenorrhea
and internal genitalia
Karyotype • 46XX • 46XY

• Normal ovaries with regular

ovulation
• Normal breast and pubic/
• Normal looking external female
axillary hair development
genitalia (but with short or
• Shortened or absent vagina
absent vagina)
Features • Absent or streak uterus
• No internal male/female genitalia
(Mullerian agenesis)
• Abdominal testes
• Renal abnormality (33%)
• Lack pubic or axillary hair
• Skeletal abnormality (12%)
• Middle ear bone defects
(deafness)
• Present
• Absence of androgen action
Breast • Present allows even low levels of
estrogen to cause breast
development
• Absent
• Absent
• (+) Miillerian Inhibiting Factor
Uterus • Failure of Mullerian duct
(MIF); synthesized in the
formation
Sertoli cells of the fetal testes
• Absent: due to lack of androgen
Pubic hair • Present
receptors
• Testes
Estrogen source • Ovaries (androgens are peripherally
converted into estrogens)
Testosterone
• Female levels • Male levels

level
• Creation of neovagina
( see Section 1 of Chapter 14)
• Can have biological children
with ART+ surrogacy or uterine
transplantation
Management
• Uterine transplant from a
compatible donor has been
done successfully resulting in
livebirths of biological offspring.
I
.
• Gonads are removed as
prophylaxis against germ cell
tumors (at around 18 years
old to allow time for full breast
development & epiphyseal
closure)
• Creation of neovagina if
patient decides to continue
on as female, (see Section 1 of
Chapter 14)

421
III. CATEGORY 3: UTERUS ABSENT AND BREASTS ABSENT (Rare)
• Reduced or absent levels of both gonadal and adrenal sex hormones result in sexual
infantilism and ambiguous genitalia in 46XYpatients
• Low estrogen and (+) MIF: check karyotype
• Conditions include:
17, 20-desmolase enzyme deficiency (46XY)
17-alpha-hydroxylase enzyme deficiency (46XY)
0Agonadism/vanishing testes syndrome (46XY)

IV. CATEGORY 4: UTERUS PRESENT AND BREASTS PRESENT

• All are karyotypica! and phenotypically female
• (+)Estrogen,(-) MIF
• Evaluate and treat like secondary amenorrhea (see below)
• Conditions include:
Hypothalamic causes
Pituitary causes
Ovarian causes
Uterine causes
Outflow tract obstruction causing cryptomenorrhea (e.g., imperforate hymen,
transverse vaginal septum, vaginal/cervical agenesis or atresia)

SECONDARY AMENORRHEA
• Absence of menses for an interval of time equivalent to a total of at least 3 previous cycles
or no menses over a 6-month period in women who have menstruated previously

I. ETIOLOGIES OF SECONDARY AMENORRHEA

ETIOLOGY
I CONDITIONS
• CNStumor & infections
• Drugs, stress, exercise, weight loss
CNS- Hypothalamic
• PCOS
• Functional hypothalamic amenorrhea
Pituitary
• Neoplastic:chromophobe adenoma, ACTHand GHsecreting adenomas
(Hypoestrogenic
amenorrhea)
• Non-neoplastic lesions: Sheehan syndrome and Simmonds disease

• Damaged ovaries secondary to infection, ischemia, surgery

• Premature ovarian failure secondary to
Ovarian
Gonadal irradiation or systemic chemotherapy
0
(Hypergonadotropic
Steroid hormone enzyme deficiency
0
hypogonadisrn)
Autoimmune disease (hypoparathyroidism, Hashimoto
0

thyroiditis, Addison disease)

• Intrauterine adhesions (IUA)
Uterine
• Uterine synechiae (Asherman syndrome)

II. MANIFESTATIONS
• Absence of menses, hot flashes, decrease in breast size, vaginal dryness
• Manifestations related to underlying causes and co-morbidities, risk of intrauterine
adhesions, current drug use (e.g., OCP), diet, weight loss, stress, exercise, etc.

422
III. DIAGNOSIS
• A stepwise approach to the work-up of secondary amenorrhea will systematically
facilitate diagnosis of its underlying cause as follows:
DIAGNOSTICTEST I REMARKS
• Pregnancy must be ruled out since it is the most common cause of absence
Pregnancy Test
of menstruation in a previously menstruating woman
Progesterone • To differentiate ovulatory from anovulatory causes by inducing
Challenge Test withdrawal bleeding from estrogen-primed endometrial lining
• Includes estradiol (E2), FSH, LH,prolactin (PRL), TSH,
Hormonal Titers
dihydroepiandrostenedione (DHEAS)
• Ultrasound, CTscan, or MRI
Imaging
• Hysteroscopy

IV. PROGESTERONE CHALLENGE TEST (PCT) FOR SECONDARY AMENORRHEA

• Progestin challenge is done to induce menstruation by giving 10 mg of progesterone (e.g.,
medroxyprogesterone acetate) orally for 5- 10 days followed by an observation period of
14 days
• A withdrawal bleed occurring within 14 days of a progesterone challenge is a positive
result which establishes presence of estrogen priming effect on the endometrium

A. Positive for Progesterone Challenge Test

Withdrawalbleeding occurs
(PositivePCT)

Anovulation

Get LHlevels
Normal or low LH J
Get TSHlevels PCOS

Normal or Low TSH LowTSH

Get Prolactinlevels Hyperthyroidism

Normal proloctin High profoctin

Hypothalamicpituitary
Hyperprolactinemia
dysfunction

DIFFERENTIALS DESCRIPTION

• Can result from any condition that disturbs the hypothalamic-

Hypothalamic- pituitary-ovarian (HPO) axis
Pituitary Dysfunction • This may be idiopathic, or may be the result of stress or excessive
weight loss (e.g., athletes or those with eating disorders)
• Although the sex binding globulin is increased, testosterone and
Hyperthyroidism
estrogen are also increased relatively
• The tonically elevated estrogen concentration then leads to a
hormonal state similar to chronic anovulation (no LH surge)
• The most common endocrinopathy in reproductive-aged women
I
Polycystic Ovary • Amenorrhea or oligomenorrhea is quite frequent
Syndrome • Persistent anovulatory state that results in a steady supply of
estrogen and the lack of progesterone's anti-estrogen effect
• Elevated prolactin inhibits GnRH by increasing the release of
dopamine from the arcuate nucleus of the hypothalamus
Hyperprolactenemia
• May be caused by either compression of the pituitary or excess
• production of prolactin from a pituitary gland adenoma
Source:Master-Hunter
T,et al.Am FamPhysician.
2006
Mciver,
B.,et al.MayoClinicProceedings;
1997
423
 8 Negative for Progesterone Challenge Test

I No withdrawal bleeding I
(Negative PCT)
I
I Get FSHlevels
I
I
Normal or Low FSH ! 1 High FSH{>30 mlU/mL)

IDoEstrogen+ Progesterone I
Challenge*
Premature Ovarian
Insufficiency
I
No bleeding I l With bleeding I
Cervicalstenosis I I Get LHlevels I Do karyotypingif
I Asherman syndrome <30 years old

Narmo/LH !
IJ towLH
Checkfor
Hypothalamic Ruleout CNStumors autoimmune disease
I amenorrhea I I (i.e., do MRI) I if >30 years old

'May give combined oral contraceptives(COC)pillsonce dailyx 10 days

DIFFERENTIALS I DESCRIPTION
• Formation of scar tissues obliterating the endometrial cavity that
Asherman prevents the occurrence of normal menstrual periods
Syndrome • Occurs most frequently after a vigorous scraping during curettage
• Endometrial tuberculosis
• Can occur after a cone biopsy or loop electrosurgical excision procedure (LEEP)
Cervical
• Although ovulation and estrogen production is present, iatrogenic
Stenosis
outflow tract obstruction results in a negative PCT

• Occurring before the age of 40, characterized by:

Premature 0 Lack of ovarian response to tropic stimulation
Ovarian
0 Lack of gonadal negative feedback
Insufficiency 0 Elevated circulating levels of FSH and LH

• Caused by necrosis of the anterior pituitary due to blood loss and

hypovolemic shock; FSH and LH are deficient
Hypopituitarism
0 Sheehan syndrome if obstetric in origin
0 Simmonds syndrome if non-obstetric
HPO • No follicular development, hence no estrogen priming of the
Dysfunction endometrium & withdrawal bleeding with PCT
• A cross-reaction between the TSH, FSH, LH (because of identical alpha
Hypothyroidism subunits) leads to a negative feedback suppressing the release of FSH
and LH affecting follicular maturation and ovulation
Source: Master-HunterT.et al. Am Fam Physician.2006, Mciver,8., et al. MayoClinicProceedings; 1997

IV. MANAGEMENT
• Management depends on the etiology of secondary amenorrhea
• Objectives of treatment may vary and some etiologies may or may not be correctable

General Principles in Management;

• Attempts to restore ovulatory function by treating underlying cause
• Hormonal replacement therapy (HRT) is given to hypo-estrogenic women
0 Estrogen and progesterone: if with uterus
0 Estrogen only: if without uterus
• Anovulatory women: cyclic progesterone
• Those with intrauterine adhesions: hysteroscopic lysis of adhesions
• Those with outflow tract obstruction: create outflow tract
• Gender reassignment, if necessary, is undertaken through an expert, multi-disciplinary approach
(e.g., psychiatric evaluation, etc.)
• For some, it may be necessary to refer these individuals to a center that offers psychiatric support
• Patients who desire pregnancy may require assisted reproductive technology

424
 SECTION TWO
MENSTRUAL ABNORMALITIES
DYSMENORRHEA
• Suprapubic pain which may occur before, during, and even after the menstrual flow
• Often accompanied by other symptoms (e.g., sweating, tachycardia, headache, nausea)

I. ETIOPATHOGENESIS
A. Pathogenesis
0 There is a close association between dysmenorrhea and elevated prostaglandin F2a
(PGF2a) levels
0 During menses, myometrial contractions decrease uterine blood flow and cause
ischemia and sensitization of pain fibers

B. Factors Affecting Dysmenorrhea

0There is a significant positive correlation between the severity of dysmenorrhea, the
duration and amount of menstrual flow, and early menarche
0There is a genetic predisposition to conditions (physiologic or pathologic) that brings
about dysmenorrhea

C. Primary vs Secondary Dysmenorrhea

I PRIMARY DYSMENORRHEA I SECONDARY DYSMENORRHEA
• Idiopathic menstrual
pain without identifiable
pathology, often occurring
Definition with the initiation of ovulatory
menstrual cycles
• Pain with no obvious
pathologic pelvic disease
• Thought to result from uterine
contractions due to increased
endometrial prostaglandin
Etiology
production derived from the
arachidonic acid pathway
during menstruation
• History of non-progressive
dysmenorrhea in the absence
of organic causes.
Diagnosis
• Occurs with ovulatory cycles
on the first or second day of
menstruation
• Progressive painful menses
due to an underlying pathology
(e.g., endometriosis, fibroids,
adenomyosis, pelvic inflammatory
disease [PIO], cervical stenos is)
• Due to uterine cramps from
increased prostaglandins released
in response to certain conditions
(e.g., endometriosis, adenomyosis)
during menstruation
• History of progressive
dysmenorrhea with coexisting
gynecologic conditions
• Increasing pelvic pain starting
before menstrual flow that may
persist after
• Most often seen in women >20

■
Age • Almost always occurs in
years old (but may occur in those
predilection women <20 years old
younger)
• No obvious abnormalities
• Structural abnormalities on
except a generalized
Examination bimanual examination and pelvic
tenderness throughout the
ultrasound
pelvis
• In endometriosis: dyschezia and
dyspareunia
Associated • Nausea, vomiting, and
• Other associated symptoms vary
Symptoms headache
with the etiology of the secondary
dysmenorrhea

425
II. APPROACH TO DIAGNOSIS
APPROACH I REMARKS
• Diagnosis is made predominantly by history and physical examination
• Typical complaint is midline, crampy, lower abdominal pain which begins with
History the onset of menstruation and gradually resolves over 12-72 hours
• Pain does not occur at times other than menses and only occurs in ovulatory
cycles

• Do bimanual exam (vaginal and/or rectal) on adult patients and only

Examination abdominal examination on adolescents
• Those with primary dysmenorrhea have a normal pelvic examination
• Always rule out for causes of secondary dysmenorrhea
Other tests • Do ultrasonography
• Laparoscopy with or without biopsy may be needed

III. MANAGEMENTOF DYSMENORRHEA

A. Treatment of Primary Dysmenorrhea
Nonsteroidal anti-
inflammatory drugs
(NSAIDs)
Non-pharmacologic
therapy
• First-line therapy for primary dysmenorrhea
• Prostaglandin synthetase inhibitors which alleviate symptoms
• Exercise: releases endorphins and improves blood flow; has been
shown to reduce severity and duration of dysmenorrhea
• Heat (patch or wrap)
• Behavioral interventions (e.g., Lamaze exercises)

• Oral contraceptives
Other therapies • Other analgesics
• Transcutaneous electrical nerve stimulation (TENS)

B. Treatment of Secondary Dysmenorrhea

1. Estrogen Suppression
• Since most pathology of secondary dysmenorrhea are estrogen dependent
• Medical treatment is directed against further estrogen stimulation
• This is achieved by medically inducing any of the following:
• First-line medical treatment
• COCpills or progesterone-only contraception (pills, injectables,
Pseudopregnancy
intrauterine device (IUD), or implants)
state*
• May be given continuous or cyclical
• Affordable, easily accessible, and well-tolerated

• Second-line medical treatment

• GnRH agonists
Pseudomenopausal • May cause menopausal side effects (e.g., hot flashes, vaginal
state** dryness, loss oflibido, mood swings, bone mineralization diseases)
• May require "add-back" therapy: addition of estrogen+/-
progesterone to alleviate GnRH-induced menopausal symptoms

• Danazol, a synthetic derivative of testosterone

• Unacceptable androgenic and anabolic effects (e.g., weight gain,
Pseudovirilized edema, myalgia, acne, oily skin, hirsutism, deepening of the voice)
state*** has limited its use
• No longer recommended
• Vaginal route (for localized effect) being studied
•Pseudo-pregnancy state: the progestin component induces secretory transformation,decidualization,and
finallyatrophy of the endometrioticlesions as what typicallyhappens during pregnancy
"Pseudo-menopausal state: a state of hypogonadotropichypogonadalanovulationsecondary to pituitary
desensitizationand reduced secretion of LHand FSH
... Pseudo-virilizedstate: the inductionof a state of 'androgen excess" that inhibitsmidcycleFSHand LH
surges and decreased steroidogenesis in the ovaries

426
 2. Pain Control
• NSA!Ds (e.g., mefenamic acid, ibuprofen, diclofenac, naproxen): analgesics of choice
because of its anti-prostaglandin properties

3. Conservative/Definitive Surgery
ETIOLOGY I MANAGEMENT
• Laparoscopic fulguration of endometriotic mplants
• Oophorocystectomy
Endometriosis • Presacral neurectomy
• Hysterectomy: reserved for those refractory to medical
treatment and conservative management, or fertility not desired
• Removal of adenomyotic lesions (Osada technique),
Adenomyosis
hysterectomy
Pelvic adhesions • Laparoscopic adhesiolysis
Cervical stenosis • Dilation of the cervix

PREMENTRUAL SYNDROME & PREMENSTRUAL DYSPHORIC DISORDER

• Characterized by a constellation of physical and/or behavioral changes that occur in the
second half of the menstrual cycle

I. ETIOPATHOGENESIS
• Unknown cause, but is likely multifactorial (physiologic and psychological)
• Women with PMS and PMDD may have an abnormal response to normal hormonal changes
• Syndrome is likely attributed to estrogen excess

TERM I DEFINITION
Premenstrual • Group of mild/moderate symptoms that occur in the second half of
Syndrome (PMS) the menstrual cycle
• More severe disorder
• With marked behavioral and emotional symptoms
• PMDD (in contrast to PMS) has the following characteristics:
Premenstrual , More severe
Dysphoric 0 Must have one severe affective symptom ( e.g., markedly
Disorder (PMDD) depressed mood or hopelessness, anxiety or tension, affective
]ability, or persistent anger) which occurs regularly during the
last week of the luteal phase
0 Substantial impairment in personal functioning
Source:Gershenson
DM,et al. Comprehensive
Gynecology;
2021

II. MANIFESTATIONS

■
• Irritability, anxiety, depression
• Symptoms are followed by a period entirely free of symptoms
Symptoms
• PMDD and PMS are similar in that symptoms manifest in the luteal
phase of the menstrual cycle and resolve during menses
Signs • Breast tenderness, bloating, headache
Source:Gershenson
DM,et al. Comprehensive
Gynecology;
2022

427
III. DIAGNOSIS (CRITERIA)
• Symptoms must occur in the 2 weeks prior to menstruation and resolve following onset
of menses
• There must be at least a 7-day symptom-free interval in the first half of menstrual cycle
• Symptoms must occur in at least t'No consecutive cycles for the diagnosis to be made.

IV. MANAGEMENT

• Exercise and relaxation techniques

Non-
• Complex carbohydrate-rich beverages improve psychological and
Pharmacologic
appetite cravings by modulating tryptophan and serotonin synthesis
• Selective serotonin reuptake inhibitors (SSRis): first line of treatment
(e.g. fluoxetine, sertraline, paroxetine, and citalopram)
• Serotonin/norepinephrine reuptake inhibitors (SNRis) (e.g. venlafaxine)
• Vitamin supplementation:
Pharmacologic 0
Calcium (600 mg BID)
0
Vitamin D3 (800 IU/day)
0
Vitamin B6 (up to 100 mg/day)
0
Magnesium (200 to 360 mg/day)
0
Chasteberry extract (one tablet per day)

428
 SECTION THREE
ABNORMAL UTERINE BLEEDING

OVERVIEW OF ABNORMAL UTERINE BLEEDING (AUB)

• Abnormal menstruation is one of the more common reasons for gynecologic consult
• Almost all women at some point in their lives will experience menstrual bleeding that will
be perceived to be abnormal

FIGOAUB System: Nomenclature and Definitions of AUB Symptoms

• In the assessment ofa patient who complains of abnormal bleeding patterns, the
frequency, duration, regularity and flow volume of menses should be determined
• lntermenstrual bleeding and bleeding while on hormonal treatment should also be quantified
• Any parameter that deviates from the "normal" as defined in the table below should be
considered "abnormal" and should warrant further investigation

PARAMETER NORMAL ABNORMAL I

CHECK I
• Absent (no bleeding) = amenorrhea □
• Infrequent (>38 days) □
Frequency
• Normal (24 to 38 days) □
• FI:equent (<24 days) □
• Normal (,;;8 days) □
Duration
•-Prolonged (> 8 days) □
• Normal or "Regular"
(shortest to longest cycle variation:,:; 7-9 days)* □
Regularity
• Irregular
(shortest to longest cycle variation:<!: 8-10 days)* □

• Light □
Flow volume
(patient • Normal □
determined)
• Heayy □

• None □
Intermenstrual
Bleeding (1MB) 1,• Random □

Bleeding between
• Early Cycle □
cyclically regular • Cyclic (predictable) • Mid Cycle □
onset of menses
• Late Cycle - □

■
Unscheduled • Not applicable (not on gonadal steroid medication) □
Bleedin~on
Progestm +/- • None (on gonadal steroid medication) □
Estroi:en Gonadal
Stermds** • Present □

'Usingthesecriteria,thenormalrange(shortest
to longest)
varieswithage:
18-25yearsofage:,:;gdays
0 26-41yearsofage:$7 days
0 42-45yearsofage:,:;gdays
"Progestin+/-estrogen gondalsteroids
mayincludebirthcontrolpills,rings,patches,
orinjections)

Source:MunroMG,CritchleyHO,Fraser,IS IntJ GynecolObstet2018

429
FIGO (PALM-COEIN) CLASSIFICATION SYSTEM OF AUB
• Classification system with a standardized nomenclature intended to be used worldwide
by researchers/clinicians investigating & treating women of reproductive age with AUB
• There are nine main categories, arranged according to the acronym PALM-C0EIN

l
~ l
IStructural I INon-structural I
1 1
!'_olyp !; oagulopathy
~ denomyosis Q vulatory dysfunction
~eiomyoma ;_ ndometrial

Malignancy and ! atrogenic

hyperplasia !:!!_ot yet classified

• Components of the PALMgroup are discrete (structural)entities that can be measured visuallywith
imaging techniques and/or histopathology
• The COEIN group is related to entities not defined by imaging/histopathology(non-structural)

I. STRUCTURAL AUB
ETIOPATHOGENESIS
I MANIFESTATIONS I MANAGEMENT

Ed 1 (AUB-P)
n omet r,a IP oyp ~

• Localized overgrowths of endometrial

• lntermenstrual
tissue, containing glands, stroma, &
bleeding
vessels, covered with epithelium • Hysteroscopic
• Diagnosis: ultrasound,
• Histology: endometrial glands, polypectomy
hysteroscopy, and
endometrial stroma, and central
histologic studies
vascular channels
--_-,!, ..
Adenqmyosls(AVB.-11.) - --
• Heavy menstrual • Analgesics
• Presence of endometrial glands and
bleeding and • GnRH agonists
stroma in the uterine myometrium
secondary • Levonorgestrel
• Histology: endometrial components
dysmenorrhea intrauterine system
seen histologically at least 2.5 mm
• Diagnosis: ultrasound, • Adenomyomectomy
beneath the endomyometrial junction
MRI, histologic studies or hysterectomy
Lelomyomaor Fibic,ids
(AUIJ_-1,) ,
~-"'
• Fibroid masses that push • GnRH agonists
• May be associated with
normal uterine musculature • Selective
heavy bleeding, pressure
outwards creating a surrounding progesterone
symptoms, or pain
pseudocapsule around it receptor
• Depending on location:
• Possible cause: somatic mutation in modulators
intramural, submucous,
a single progenitor cell which may be • Myomectomy
subserous, others
affected by estrogen & progesterone • Hysterectomy
tfaligna,rf:y ~,. Hyjer¢asia (:A_riB-Mj' 'ii ,~
• Premalignant endometrial • High-dose
• AUB is the most
hyperplasia results from prolonged progesterone
common presenting
unopposed estrogen exposure • Endometrial
symptom of
• Adenocarcinoma is one of the most ablation
endometrial
common malignancies in the female • Definitive: surgery
hyperplasia and cancer
genital tract (sarcomas are rarer) • Chemo/radiotherapy

430
II. NON-STRUCTURAL AUB
ETIOPATHOGENESIS
I MANIFESTATIONS
I MANAGEMENT

Coagulopathy (APB·C)
-
• Encompasses a spectrum
• As seen in systemic disorders such
of systemic disorders of • Treatment of
as von Willebrand disease and
hemostasis that may be underlying cause
prothrombin deficiency
associated with AUB
Ovul;,t'ory Dysfunction, (AUB-O) .,
""
• Includes ovulatory disorders at
extremes of reproductive age • Oligomenorrhea
• Cyclic
• May be secondary to alterations in • lntermenstrual bleeding
progesterone
neuroendocrine function (e.g., PCOS, • Heavy menstrual
• Combination OCPs
hypothyroidism, prolactinemia, obesity, bleeding
mental stress, extreme exercise)
Primary Endometriill l)isorder (:AUJ!·EJ
• Excessive uterine production • Primary disorder of the
ofprostacyclin, a vasodilatory endometrium when AUB • LNG-IUSmay be
prostaglandin that opposes platelet occurs in a predictable & helpful
adhesion and may also interfere cyclic manner, typical of • NSAIDs
with uterine contractility ovulatory cycles
A
Iatrogenic (AUB•I)
• Due to medications such as SERMs,
GnRH analogues, anti-coagulants,
• Tailored to the
risperidone and other antipsychotics • Depending on cause
specific cause
• Uterine perforation or laceration
associated with surgical procedures
!Jot other~ise clas~ified fAUB·N)
-
• Abnormal bleeding not classified in
the previous categories • Tailored to the
• Depending on cause
• Examples of such conditions may specific cause
include foreign bodies or trauma
Source:MunroMGet al IS IntJ GynecolObstet2018

431
 The FIGOSystem Categories of Myomas
• This is the FIGO
leiomyoma
subclassification
system that includes a
tertiary classification
ofmyomas
• It further categorizes
submucous and
subserous myomas
based on the ratio of
the myoma located
intramurally

0 Pedunculated intracavitary
SM-SUBMUCOUS 1 <50% intramural
2 ;,SQ% intramural
UNCLASSIFIED 3 Contacts endometrium; 100% intramural
4 Intramural
5 Subserous ;,50% intramural
0 -OTHER 6 Subserous <50% intramural
7 Subserous pedunculated
8 Other (specify e.g., cervical, parasitic)
Submucous and subserous, each with less than half the
2-5 diameter in the endometrial and peritoneal cavities,
respectively
HYBRID
'Twonumbersare listedseparatedbya hyphen.Byconvention, the firstrefersto the
relationship
withthe endometriumwhilethe secondrefersto the relationship to the
serosa.Oneexampleis above.
Source:MunroMG.et al. J GynaecolObste;2018

Example of Annotating Causes of AUB using the PALM-COEINNotation

• Formal approach follows the WHO TNM staging of malignant tumors, with each
component addressed for all patients. In all cases, the presence or absence of each
criterion is noted using "O"if absent, "1" if present, and"?" if not yet assessed.
• Other examples:

AUBP,AOLOMO- AUBP0 A1 L0 M0 - AUBPOA0 L,[sMJ

M0 -
co0 0 E0 10 N0 C0O0 E0 !0 N0 C0 0 1 E0 10 N0
Abbreviated: AUB-P Abbreviated: AUB-A Abbreviated: AUB-L,O

endometrial polyp adenomyosis, ovulation dysfunction (PCOS),

focal and/or diffuse and submucosal leiomyoma

432
APPROACH TO ABNORMAL UTERINE BLEEDING
I. DEFINITION OF ABNORMAL UTERINE BLEEDING (AUB)
• Includes any significant deviation from normal menstrual bleeding patterns attributed to
the uterine corpus
• AUBmay include (with or without any recognizable pathology):
Short or long (but regular) cycles
, Irregular cycles
Heavy /light periods
, lntermenstrual bleeding
, Premenarcheal or postmenopausal bleeding
• Heavy menstrual bleeding is defined as excessive menstrual blood loss which interferes
with the physical, emotional, social and quality of life, and which can occur alone or in
combination with other symptoms
ONSET I DEFINITION
• An episode of heavy bleeding sufficient in quantity to require immediate
AcuteAUB
intervention to prevent further blood loss
• Present for the majority of the past 6 months
ChronicAUB
• Usually does not require immediate intervention

II. DIFFERENTIALS
ONSET OF MENORRHAGIA I PROBABLE DIAGNOSIS
• Immediately after menarche • Physiologic: anovulation, perimenopausal
• Late 40s & SOs transition
• Since onset of medication
• Medication-induced
• Soon after medication
• Weight gain or symptoms of hyperandogenism • Anovulation (e.g., PCOS)
• Gradual increase over months or sudden & • Myoma
noncyclic • Hyperplasia or carcinoma
• Increasing disability from systemic disease • Chronic disease

III. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Pregnancy test or sensitive ~-hCG assay
• CBCand coagulation profile (adolescent & older women)
• Thyroid function tests (TSH, FT3, FT4)
Basic tests
• Pap smear
• Screening for ST!
• Serum ferritin
• Ultrasonography: first-line diagnostic tool
Imaging
• Saline infusion sonography (SIS): accurate evaluation tool for
studies
intracavitary lesions

■
• Postmenopausal woman with bleeding or premenopausal woman with
heavy /irregular vaginal bleeding
EndometriaI • Postmenopausal women with endometrial cells on pap smear
biopsy • Premenopausal women with atypical glandular cells on pap smear
• Breast cancer patients on tamoxifen with abnormal vaginal bleeding
• Women who are still "menstruating" after 52 years of age
• Gold standard
Hysteroscopy • Both diagnostic & therapeutic
• Targeted biopsy more accurate than D&C
Sources:NICEguidelinesfor heavymenstrualbleeding,2007
MunroMGel al. IntJ GynecolObstel2018
CPGonAbnormalUterineBleeding,POGS,Inc.:2017.
433
IV. MANAGEMENT
• In general, structural etiologies for AUB (PALMfrom the PALM-COEINSystem) generally
require surgical correction
• Therapy for non-structural causes of AUB (COEINfrom the PALM-COEIN System) should
be tailored to address the specific underlying cause when a cause is identifiable

A. Management of Acute AUB

DRUG I REMARKS I DOSAGE
• Endogenous estrogen source that
• For unstable patients:
High dose rapidly proliferates the denuded
25 mg IV every 4 hours up
conjugated endometrium
to 24 hours, or
equine • Contraindicated in patients with
estrogen • For stable patients: 2.5 mg
history ofDVTand pulmonary
PO every 4 hours
embolism
• The estrogen component causes rapid
• Combined monophasic
growth of the endometrium while the
OCPs containing 35 mcg
Combined progestin component stabilizes the
ethinylestradiol given
monophasic endometrium so that an organized
TID x 3 days, then BID x 2
OCPs slough occurs after the withdrawal
days, and then OD for the
• Option for stable patients when oral
remainder of the pack
equine estrogen is not available
• High dose progestin exerts a
stabilizing effect on the endometrium • Medroxyprogesterone
Oral • May be given during acute bleeding 20 mg OD x 10 days or
progestogens that is not extremely heavy (in • Norethindrone 20 mg TID
which case, estrogen is the preferred x 7 days
treatment)
• Anti-fibrinolytic agent that inhibits
• Tranexamic acid
Tranexamic fibrinolysis
1 g PO every 6 hours
Acid • Best given to patients with heavy
x 3-5 days
ovulatory bleeding
Source:CPGon AbnormalUterineBleeding,POGS,Inc.:2017.

B. Surgical Options for AUB

SURGERY I REMARKS
• Treatment of choice in women with hypovolemia
Endometrial
• Acute heavy menstrual bleeding (HMB) unresponsive to initial
curettage
medical management
• Polypectomy
• Myomectomy
Hysteroscopy • Edometrial ablation
0 With medical contraindication to hysterectomy
0 No longer desirous of future pregnancies

• Performed as indicated after definitive diagnosis

Hysterectomy • Cases with failed pharmacological treatment
• Women no longer desirous of future pregnancies

434
A. Long-term Management for AUB {depends on underlying cause)

~
UNDERLYING
CAUSE

Structural Causes .
Polyps --- • Polypectomy
• GnRH agonist
• Adenomyomectomy
Adenomyosis • Levonorgestrel intrauterine
• Hysterectomy
system (LNG-IUS)
• Hormonal suppression • Myomectomy
• GnRH agonist • Uterine artery embolization
Leiomyomas • Selective progesterone • MRI guided focused
receptor modulator* ultrasound
• Tranexamic acid • Hysterectomy
• Hysteroscopy with
endometrial curettage
Endometrial • Extrafascial hysterectomy
• Progestin therapy
hyperplasia with bilateral salpingectomy
(EHBS) ± bilateral
oophorectomy
• lfyoung and desirous of
• Extrafascial hysterectomy
fertility, provided early stage
with bilateral
and satisfies criteria** for
salpingooophorectomy
Endometrial cancer conservative management
(EHBSO)+ lymph node
• May give high dose
dissection
progestins and LNG-IUSwith
• Chemotherapy /radiotherapy
close surveillance
Non-structural Causes
- -
• Thyroid hormone replacement for hypothyroidism
Thyroid disorder
• Anti-thyroid medications for hyperthyroidism
Hyperprolactinemia • Dopamine agonists: bromocriptine, cabergoline
• Combined estrogen/progestin pills, patch, or ring
Anovulation • Cyclic progestin
• LNG-IUS
Primary
endometrial • NSAIDs
disorder
'As of September2020,the EuropeanMedicines Agency'sRiskAssessmentCommittee· (PRAG)has
recommended the revocationof PharmacovigilanceMarketing Authority
forthe 5 mgoraltabletsof ulipristal

■
acetateafter5 cases of severeliverinjuryneedinglivertransplantwerereported

"Criteriaforconservativemanagement:
0Well-differentiated
tumor(Grade1, endometrioidtype)
0Nomyometrial invasion,
cervical,
adnexal,parametrial
andvaginalinvolvement
onMRI
0Nosuspicious retroperitoneal
lymphnodesor noevidenceoflymphnodemetastasis
0NegativePFC
0Nolymphovascular space invasion(LVSI)
0Nocontraindications formedicalmanagement

435
 SECTION FOUR
POLYCYSTIC OVARY SYNDROME

POLYCYSTIC OVARY SYNDROME (PCOS)

• Originally described as a syndrome consisting of amenorrhea, hirsutism, and obesity in
association with enlarged polycystic ovaries
• Classic definition includes women who are anovulatory and have irregular periods and
hyperandrogenism (e.g., hirsutism, elevated androgens)
• Lifetime disease of which the management mainly consists of controlling its effects and
preventing its potential consequences.

I. ETIOPATHOGENESIS
• Previously known as the Stein-Leventhal Syndrome
• Most common endocrinologic disorder among women of reproductive age

A. Risk Factors
0Associated conditions: diabetes, obesity, heart disease, endometrial cancer

B. Pathophysiology
0 Poorly understood

, Primary problem may lie in the hypothalamus, the pituitary, the adrenals, the ovaries,
or even the adipose tissues

MECHANISM I EFFECTS
• Results in increased production of LHby the pituitary
• Constant elevation of LH in turn prevents the occurrence of an LH surge
Increased that promotes anovulation, leading to:
frequency of 0 Incomplete follicular development resulting in the polycystic ovarian
GnRH pulsatility morphology and increased androgen production by ovaries
0 Elevated estrogen milieu and an absence of the physiologic
production and withdrawal of progesterone
• Androgen brings about insulin resistance that leads to a compensatory
insulin hypersecretion:
Insulin 0 Promotes further androgen output by the ovaries and adrenals
Resistance 0 Suppress hepatic production of sex hormone binding globulin
(SHBG),which exacerbates hyperandrogenemia by increasing the
proportion of free circulating androgens and estrogens
Source: SperoffL, et al. ClinicalGynecologicEndocrinology 2011
and Infertility;

II. MANIFESTATIONS
A. Features of PCOS
0 Manifestations include menstrual disorders, androgen excess, and difficulties in conceiving
0 Presents with hirsutism, virilization, anovulation, amenorrhea, and obesity
FEATURES I REMARKS
• For the ovaries to be labelled polycystic, 12 or more cystic follicles
Polycystic Ovaries measuring 2-9 mm in diameter or an ovarian volume of>l0 cm3 will have
to be documented by transvaginal or trans rectal ultrasound
• Majority (68-85%) have abnormal menstruation
Anovulation
• Oligomenorrhea and amenorrhea: most frequently experienced
• Clinical manifestations may include hirsutism, acne, alopecia, truncal
obesity, and acanthosis nigricans
• Biochemical abnormalities for androgen excess:
Hyperandrogenism
Elevated serum free testosterone
0

Decreased SH8G
0

Increased computed free androgen index

0

Source:TeedeHJ, et al. HumReprod,2018

PCOS ConsensusWorkshopGroup;2003
RotterdamESHRE/ASRM-sponsored

436
 B. Androgen Excess(Hyperandrogenism) in Females
0 Hirsutism (60%): primary clinical indicator of androgen excess
0 Virilization: characterized by masculinizing and anti-estrogenic effects of testosterone
0 Other manifestations ofhyperandrogenism include acne and androgenic alopecia

I HIRSUTISM I VIRILIZATION
• Mild forms: upper lip & chin
• Characterized by masculinizing
• More severe forms: cheeks,
and anti-estrogenic effects of
intermammary, chest,
testosterone
abdomen, thighs, back,
• Temporal balding, clitoral
Features intergluteal areas
hypertrophy
• May have normal ovulatory
• Reduced breast size
menses
• Vaginal dryness
• Usually have oligo or
• Increased muscle mass
amenorrhea
Onset • Gradual • Abrupt
Severity of
• Normal, or mild to moderately • Marked elevation of circulating
Androgen
excess elevated (<1.5 ng/mL) testosterone (>2 ng/mL)

Ill. DIAGNOSIS
• There are three Consensus Diagnostic Criteria for PCOS
• Some women with PCOSmay not have menstrual irregularity, so the Rotterdam criteria
emerged, which is most widely used for PCOS
• The Rotterdam Criteria is used locally to guide in the diagnosis of PCOS

A. ConsensusDiagnostic Criteria for PCOS

2003 ESHRE/ASRM 2006 Androgen Excess
1990 NIH

Requires both Criteria

I (Rotterdam Criteria)
Requires 2 of 3 Criteria
I Society (AES)
Requires all 3 Criteria
Menstrual Menstrual irregularity Ovarian dysfunction
1 irregularity (chronic 1 (oligo- or anovulation) 1 (oligo-ovulation and/
anovulation) or PCO)
Clinical and/or Clinical and/or Hyperandrogenism
2 biochemical signs of 2 biochemical signs of 2 (hirsutism and/or
hyperandrogenism* hyperandrogenism* hyperandrogenemia)
Polycystic ovaries Exclusion of other
3 3 androgen excess
disorders
•Exclusion
ofotherandrogenexcessdisordersinthosewithclinicalhyperandrogenism is important
to ruleout
othercausesofandrogenexcess(e.g.,congenital
adrenalhyperplasia,Cushingsyndrome,adrenaltumor,drug
inducedandrogenexcess,& producingovariantumor)beforehyperandrogenism is attributedto PCOS
Source:NIHconference,Bethesda;1990
Rotterdamcriteria,ESHREandASRM;2003 ,
■·
AndrogenExcessSociety;2006
TeedeHJ,et al. HumReprod,2018

437
Ferriman-Gallwey Scoring System:
(helpful in evaluating and quantifying the pattern and extentofhirsutism in PCOS)

•
Upper
lips @-
~
~ (0-·®-·
,,.,, tt> c,r,, ,,<t>

;;;:
a., ,.~
0,
(0~®- ®··- ®.:.
<$'-, ,~

e$
- ~- a.,
::.
,.-i, a.,
::.
,11;> <T>,,•.._.

.:;;:.
<t•• ,,,c,
:;;:.
ch·in

1 2 3 4 1 2 3 4

Che~ fV:W,
v/v~v~,
1 2 3 4

~:::~.f
1 2 3 4

rlitlf
+1
;~;:~.,t\f 1 2 3 4

Back f'f'ffi\::
1 2 3 4

Acms il I\ I\f'
1 2 3 4

Thighs wwww 1 2 3 4

Buttocks ( +) (+) ('r) ft0

1 2 3 4
Hirsutism cut-off:
• >7or 8 (Caucasians
or African-Americans)
• >3(Asians)
Source:Ferriman-Gallwey
scale,modifiedby Hatch;1981

438
 B. Diagnostic Considerations For Adolescents
For adolescents, polycystic ovarian morphology and anovulatory symptoms may not
be enough to make a diagnosis of PCOSsince these may be normally seen in the early
period of reproductive maturation
Diagnosis of PCOSin this age group may be established based on:
• Oligomenorrhea, AND
• Clinical and/or biochemical evidence of androgen excess
Ultrasound is not recommended in diagnosis in patients <8 years post menarche

C. Diagnostic Approach for PCOS

Irregular cycles+ clinicalhyperandrogenism?

Excludeother causes ➔ diagnosis

l
If no clinicalhyperandrogenism
Test for biochemicalhyperandrogenism Menstrual
(excludeother causes) ➔ diagnosis irregularities

l
If ONLYirregular cycles ORhyperandrogenism PCOS PCOS
(B) (O)
PCOS
Adolescent: ultrasound not indicated ➔ (A)
consider at risk of PCOSand reassess later
PCOS
Androgens (C) Ultrasound
Adults: request ultrasound for PCOM
If positive (oxcludeother causes) ➔ diagnosis

l
Classifythe phenotype
Phenotypization
PhenotypeA:has all 3 criteriaof Rotterdam.
PhenotypeB:has 2, menstrualirregulari!ies and hyperandrogenism (clinicalor biochemical)
PhenotypeC: has 2, hyperandrogenism (clinicalor biochemical)
and polycystic ovarieson ul!rasound
PhenotypeD:has 2, menstrualirregularities and polycysticovarieson ul!rasound

Theneed forphenotyping highlights

!hefactthatnotall PCOSpatientsclinicallypresentthe same way.
Phenotypingwillavoidunderdiagnosing and guidetreatment.Although
all patientswillhavea basiccomponentin
itstreatment,directedmanagementof the symptomswilldependon the phenotype.
Source:TeedeHJ,et al. HumReprod.2018

IV. MANAGEMENT
With the problem probably lying primarily on the hormonal regulation by the
hypothalamus plus the involvement of many other organs, it should be considered a
multisystemic disorder
• Treatment depends in the particular symptoms and the desires of the patient

■
• Management goals consist of: .
Restoration of normal menstruation
Improvement of fertility
, Lowering of insulin resistance levels
Treatment of hirsutism, alopecia or acne
, Prevention of endometrial hyperplasia, DM, and cardiovascular disease

A. First Line Therapy: Lifestyle Modification

0 Moderate weight loss thru dietary modifications

0 Regular exercise

439
B. Interventions Based on Symptomatology
DESIROUS OF
SYMPTOM

Abnormal
I PREGNANCY I NOT DESIROUS OF PREGNANCY

• First line: cyclic progestogen • First line: combined oral contraceptives

Uterine
• Second Line: metformin • Second line: metformin
Bleeding
• First line: letrozole,
clomiphene
Infertility • N/A
• Second line: gonadotropins,
ovulation induction, IVF
Insulin
• Metformin • Metformin
Resistance
• Combined oral contraceptives,
Acne • Topical creams topical creams, antiandrogens
(spironolactone)
• Electrolysis and light based therapies,
• Hair removal techniques
Combined oral contraceptives with
Hirsutism [electrolysis, lasers, and
or without anti-androgen therapy
intense pulsed light)
(Spironolactone)

C. Specific Pharmacoiogic Treatment of PCOS

DRUG
I MECHANISM
I INDICATIONS I DOSAGE
• Increases SHBG • Androgen
Combined oral • Suppresses LH and symptoms
• Cyclical or continuous
contraceptives FSH • Menstrual
• Antiandrogen irregularity
• Primarily
for insulin
• Reduces hepatic
resistance
glucose production,
• Relative • Dose: 1500 mg/day
lowering insulin
indications: (started at 500 mg BID,
levels
Metformin androgen then titrated upward as
• Possible
symptom, tolerated; with 500 mg
improvement
menstrual weekly increments)
in ovarian
irregularity,
steroidogenesis
ovulation
induction
• Start with 2.5 mg per day
x 5 days, beginning
• Ovulation
• Aromatase inhibitor Day 2-5 of menses; with
Letrozole induction
• Increases FSH 2.5 mg increments*
[off-label use)
• Maximum dose:
7.5 mg/day
• Start with lowest available
• Antiestrogen dose (SO mg), with SO mg
Ciomiphene • Ovulation
• Acts to induce rise in increments*
citrate induction
FSH and LH • Maximum dose:
200 mg/day
• Androgen
• Inhibit androgens
symptoms (e.g. • Spironolactone:
Anti-Androgens from binding to the
hirsutism, acne, 25-200 mg/day
receptors
oily skin)

'If folliculardevelopmentwiththe previousdose is not detecled in the previouscycle

Sourcesfor thispage:LegroRSet al. Guidelines on PCOS.J ClinEndocrinolMetab;2013
TeedeHJ,et al. HumReprod.2018
Tayloret al. SperotrsClinicalGynecologic
Endocrinology andInfertility,
2019
440
V. Long-Term Medical Sequelae of Untreated PCOS
• If not treated, PCOSwill expose patients to a metabolic and hormonal milieu that will
predispose these women to possible long term medical sequelae
SEQUELAE I REMARKS
• Increased visceral adiposity or waist-to-hip ratio
Obesity or
• Associated with hyperandrogenemia, insulin resistance,
overweight
glucose intolerance and dyslipidemia
Impaired Glucose
Tolerance and • Patients with PCOSare more insulin resistant
Type 2 Diabetes
• Testosterone decreases lipoprotein lipase activity in
abdominal fat cells
• Insulin resistance impairs the ability of insulin to exert its
antilipolytic effects
Dyslipidemia
• End results:
0 Hypertriglyceridemia
0 Increased levels of low-density lipoproteins (LDL)
0 Decreased levels of high-density lipoproteins (HDL)
Vascular • Hypertension due to reduced vascular compliance and
Dysfunction and vascular endothelial dysfunctions
Coronary Disease • Increased risk of coronary artery atherosclerosis
• Due to anovulation, the unabated production of estrogen and
Endometrial the absence of the much-needed protection afforded by the
Hyperplasia and cyclical progesterone production and withdrawal results in
Malignancy continued stimulation of the endometrial lining which may lead
to endometrial hyperplasia and possibly malignant changes
• The anovulation and the endometrium characteristic of
PCOSare neither conducive to conception nor supportive of
Subfertility or implantation leading to difficulties in getting pregnant for a
Infertility number of these patients
• Related obesity has been found to directly correlate with
ovulatory dysfunction and inversely with fertility
Psychiatric • Increased prevalence of eating disorders, anxiety, panic attacks
Problems and depression
is recommended
subspecialists
Referralto appropriate dermatologic,
forotherconcerns(e.g.,metabolic,
psychiatric,etc.)
Source:LegroRSet al. Guidelines on PCOS.J ClinEndocrinol Metab;2013
TeedeHJ,et al. HumReprod,2018
Gynecologic
Tayloret al. SperotrsClinical Endocrinology 2019
and Infertility,
LegroRS,et al.AmericanJournalof MedicineDecember; 2001
SalenA.HumReprodUpdate;2001

441
 SECTION FIVE
INFERTILITY
OVERVIEW OF INFERTILITY

I. DEFINITION OF TERMS
• Applied only to an individual who has some absolute factor preventing
Sterility
pregnancy
• The inability of a couple to achieve pregnancy after one year of regular
Infertility
unprotected coitus
Primary • Refers to a woman who has never conceived despite unprotected
infertility coitus for at least 12 months
Secondary • Refers to a woman who has previously conceived but unable to
infertility conceive again despite unprotected coitus for at least 12 months
Fecundity • Ability to achieve a live birth in one menstrual cycle
• The probability of achieving pregnancy within a menstrual cycle (25%
Fecundability
in normal couples)

II. INFERTILITYAND AGE

• The percentage of infertile couples increases with increasing age of the female partner
0 1 in 7 couples are infertile if the wife is 30- 34 years of age
0 1 in 5 is infertile if she is 35 to 40
0 1 in 4 is infertile if she is 40 to 44
• The total length of time during which conception is still possible is less in older women

III. REQUIREMENTSFOR CONCEPTION

FOR MALES I FOR FEMALES
• Intact HPG axis • Intact HPO axis
• Normal spermatogenesis • Normal folliculogenesis
• Normal reproductive anatomy • Normal ovulation
• Normal sexual function to deposit • Adequate luteal phase
spermatozoa in the upper vagina • Normal fallopian tubes
• Normal uterus

IV. FACTORSFOR INFERTILITY

FACTOR I REMARKS
Female • Ovarian factor (30%)
factors • Uterine or tubal disease (20%)
(50-60%) • Cervical. immunologic, infectious (5%)
Male factors • Poor sperm production
(40-50%) • Sperm transport
Both partners
• Both the couple have factors that contribute to their infertility
(20%)
• Defined as couples with normal ovulation and pelvic evaluation with
a normal uterus and patent tubes on hysterosalpingogram, as well as
normal semen analysis
Unexplained
• There are two potential explanations:
(10%)
0 No abnormality: couple's fertility is at the extreme lower end of
reproductive age
0 There is a cause but one that cannot be identified with existing tests

442
EVALUATION AND DIAGNOSIS OF INFERTILITY
I. HISTORY AND EXAMINATION
• Any pregnancy complications
• Previous pelvic surgery of any type or procedures to treat cervical
abnormalities
Medical • Significant dysmenorrhea
history • Dyspareunia or sexual dysfunction
• Abnormal cervical cytology
• Medical co-morbidities and use of medication
• Symptoms suggestive of endocrine disorders (e.g.,weight change, skin change)
• Genetically related illnesses
Family History • Birth defects
• History of age of menopause in female family members
• Occupational hazards
Social History
• Smoking, drinking, and drug use
Sexual History • Risks for sexually transmitted infections
• Extremes of body mass
• Skin changes, hirsutism
• Thyroid size
Physical exam • Secondary sexual characteristics
• For males: inspection of the penile shaft and urethra, palpation & ocular
inspection of the testicles
• For females: inspection of vagina & cervix & internal/bimanual examination

II. INDICATIONS FOR INVESTIGATION

• No pregnancy after 12 months of trying to conceive, OR after 6 months if:
° Female partner >35 years old
History of oligo/amenorrhea
0 History of pelvic infection
Known or suspected uterine/tubal disease
0 Severe endometriosis
Male partner with known of suspected poor semen quality
Previous history of chemotherapy or radiotherapy

III. ETIOLOGIES OF INFERTILITY

SYSTEM I CAUSES SYSTEM I CAUSES

Female Fq.ctors for Infertility Male Fact(Jrsfor Infertility
• PCOS • Crypotorchidism
Abnormal
• Advanced maternal age • Mumps orchitis
semen
Ovulatory • Premature ovarian failure • Antisperm antibodies
• Hyperprolactinemia
• Hypogonadotropic
• Hypothyroidism Endocrine.
hypogonadism
disorders
• PIO • Thyroid disease

■
• Tubal ligation
Tubal Environmental • Radiation
• Pelvic adhesions
disorders • Heat
• Endometriosis
• Klinefelter syndrome
• Congenital malformation Genetics
• Immobile cilia syndrome
• Submucosal fibroids
Uterine • Uterine Polyps • Erectile dysfuction
Sexual
• Asherman's syndrome • Ejaculation failure
dysfunction
• Luteual phase defect • Retrograde ejaculation
• Cervical stenosis • Varicocele
Structural
Cervical • Cervicitis • Vasectomy
defects
• Unfavorable mucuous • Testicular torsion

443
APPROACH TO FEMALE FACTOR INFERTILITY
I. EVALUATIONOF FEMALEFACTORINFERTILITY
• Work-up should carefully exclude ovulatory dysfunction, pelvic factor, tubal facto,; and
uterine factors

A. Establishing Ovulation
Regular menstrual cycles, midcycle pain, and menstrual molimina are strong evidences
of ovulation that can be gathered based on careful history taking
0 Other methods of documenting ovulatory cycles include the following:

OVULATION
ASSESSMENT
I REMARKS

• Progesterone has a thermogenic effect on the hypothalamus

Basal body • Involves daily recording of temperature early in the morning upon
temperature awakening
(BBT) • Biphasic pattern: the interval of the highest fertility spans the 7 day
interval immediately before the midcycle rise in BBT
• Testing for urinary LH daily, beginning 2-3 days before expected
surge (based on individual cycle length)
LHkits
• Ovulation most commonly occurs a 10-12 hours after the detection
ofLH peak
• Ultrasound monitoring of growth of a follicle and response of the
endometrium
Follicle
• Signs of ovulation: decrease in follicle size & change in its shape,
monitoring
development of intrafollicular echoes, free fluid in the cul-de-sac
• Most accurate estimate of when ovulation occurs
• Provides histologic evidence of endometrial development and
Endometrial
response to progesterone stimulation
biopsy
• Nat routinely done
• For women with regular cycles, it should be measured in the midluteal
Serum phase, 7 days before the expected time of menses, to provide indirect
progesterone evidence of ovulation as well as normal luteal function.
titers • Value >3 ng/mL implies ovulation and >10 ng/mL indicative of
adequate luteal function

B. Ovarian Reserve Testing

The following tests may be done in women >35 years old, in those with a previous
history of ovarian surgery, or in patients suspected to have low ovarian reserves
TEST I REMARKS
Anti-Mullerian • Produced by granulosa cells of pre-antral follicles
Hormone • AMH <l ng/mL may indicate a woman with a low or diminished
(AMH) ovarian reserves
• FSH> 10 miU/mL: predictive of poor ovarian response to stimulation
• FSH >20 miU/mL in a woman in her 30s can signal premature
Day3 FSH/ ovarian insufficiency
estradiol • Elevated estradiol >70 pg/mL on day 2-3 coupled with a normal
FSH may suggest advanced follicular development that is predictive
of poor response to stimulation/decreased ovarian reserve
• Visualization of antral follicle that measure 2-9 mm in each ovary
Antral Follicle
• Normal AFC:6-10 (in both ovaries)
Count (AFC)
• An AFC <6 is a marker for diminished ovarian reserve

444
C. Evaluation of Cervical Factor
1. Billing Method

I PRE-OVULATORY I POST-OVULATORY
Dominant hormone • Estrogen • Progesterone
Ferning • Good • None
Spinnbarkeit • Thin, watery, copious • Thick, viscous, scanty

2. Post-Coital Test
• Done at time of ovulation to assess penetrability of the cervical mucus by sperms
• Taken 6 to 12 hours after coitus
• A good result would show 10 or more progressive motile sperm per high-power
field (HPF)
• No longer routinely done with the availability of in vitro fertilization (IVF) and
intrauterine insemination (JUI)

D. Evaluation of the Uterine, Tubal, and Peritoneal Factors

DIAGNOSTIC I REMARKS
• Visualizes significant pathology such as
° Fibroids
0 Adenomyosis
0 Endometriosis
Transvaginal 0 Uterine septum
Ultrasound 0 Polyps
0 Ovarian masses
• A baseline ultrasound is best done on Day 2-5 of menses,
when endometrium is thin in order to visualize endometrial
pathology
• Tubal patency determined by the opacification of tubal lumen
and spillage of transcervically introduced radio opaque dye into
the pelvic cavity; done under fluoroscopy or X-ray guidance
Hysterosalpingography • Scheduled during the week following the end of menses to
(HSG) avoid irradiating a possible pregnancy
• Contraindications:
0 History of salpingitis in the recent past
0 Tenderness on pelvic exam
• Similar to HSGbut done under ultrasound guidance
• Tubal patency determined indirectly by the accumulation
Sonohysterogram of fluid in the cul de sac when media is introduced into the
uterine cavity spills into the peritoneal cavity thru one or
both fallopian tubes
• Visual evaluation of the reproductive tract
• May be done by laparoscopy, hysteroscopy, and falloposcopy,

■
where available
Endoscopy
• May establish tubal patency by chromopertubation of
methylene blue intracervically and visualization of spillage
into the peritoneal cavity during laparoscopy.

445
II. MANAGEMENTOF FEMALEFACTORINFERTILITY
A. Timed Intercourse
0 This is the scheduling of coitus during days in the menstrual cycle when achieving
pregnancy is at its highest, usually on the day of ovulation and two days before & after
0 Use of LH kit, serum progesterone monitoring, or follicle monitoring to determine best
time for coitus
B. Management of Specific Cause
ETIOLOGY
I INTERVENTION
• Intrauterine adhesions (IUA): hysteroscopic lysis of adhesions
Uterine factor
• Leiomyoma: myomectomy
Ovulatory
• Ovulation induction (see table below)
dysfunction
• Tubal surgery may be appropriate for selected cases of distal tubal disease
but if pregnancy has not occurred within 12 months of tubal surgery, in
vitro fertilization (IVF) should be discussed
Tubal factor
• IVF should be considered as the first line treatment for moderate to severe
proximal or distal tubal disease
• TB ("pipe-stem" tube): anti-Koch's treatment
Pelvic factor • Endometriosis: fulguration of implants, cystectomy, !VF,IUI
• Controlled ovarian stimulation (COS)+ JUI or IVF
• COSshould be performed with either clomiphene citrate or human
menopausal gonadotropin (HMG)
Unexplained
• The following should proceed directly to IVF because of reduced efficacy of
Infertility
COS in such women:
• Women >36 years old after failed treatment
• Women >42 years old

• Selective estrogen • Can cause symptoms

receptor modulator (SERM) of estrogen deficiency
• Competes with during treatment
• Start with lowest
estrogen-binding sites (hot nashes, vaginal
Clomiphene available dose
on hypothalamus dryness)
citrate (SO mg), with
(receptor depletion) • Associated with
(first line) 50 mg
• This leads to an increase poor endometrial
increments*
FSH, stimulates follicle development
maturation and increase • Adverse effects include
E2 production risk of multiple pregnancy
• Start with 2.5 mg • Short-acting: problems
• Aromatase inhibitor
per day x 5 days, of thick cervical mucus
• Blocks estrogen
beginning day 2-5 or a thin endometrium
Letrozole production: increases
of menses; associated with
pituitary FSH &
with 2.5 mg domiphene have not been
follicular development
increments* reported with letrozole
, Includes recombinant • Monitor with frequent
FSH & LH, and measurement of
• Starting dose:
Gonadotropins menotropins estrogen & ovarian US
150 JU with FSH
• Induces follicular • Adverse effect: ovarian
development hyperstimulationsyndrome
• Dose:1500mg/day
(started at 500 mg
• Reduces insulin • Can be considered an
BID,then titrated
Metformin resistance and directly adjunctive treatment
as tolerated; with
stimulates ovaries for ovulation
500 mg weekly
increments)
'If folliculardevelopmenl
withthepreviousdoseis notdelectedin thepreviouscycle Source:CPGon BasicInfertility.
POGS.2019.

446
APPROACH TO MALE FACTOR INFERTILITY
I. EVALUATION OF MALE FACTOR INFERTILITY

History, physical exam

Normal Abnormal
results Semen analysis x2 results

Female evaluation

Normal Abnormal

Unexplained infertility Treat female

Antisperm antibodies factor
DNAintegrity
Sperm penetration/
hemizona assay

Eliminate Hormone
gonadotoxins evaluation
No improvement With improvement

Semen analysis Treat female factors

Oligospermia,
Lowvolume Azoospermia
asthenospermia

Source:GershensenOM,et al. Comprehensive

Gynecology,
2022
A. Semen Analysis
0 Initial evaluation of male infertility should include at least 1 properly done semen analysis
• Abstinence period of 2-7 days
• Collected by masturbation into a clear wide-mouthed container
• Collected in a private room near the laboratory & examined within 1 hour
0 Parameters used to evaluate the semen include the following:
WHO Reference Values for Human Semen
PARAMETER I DEFINITION I NORMAL VALUES
Semen volume • Amount of semen produced • .el.5 mL

■
Sperm count • Number of sperm in ejaculate • >39 million
Sperm concentration • Number of sperm per volume • >15 X 10 6/mL
Total motility • Proportion of sperm that can swim • 2!40%
Progressive motility • Sperm swimming in one linear direction • ;,32%

Morphology • Size and shape of sperm • 2:4% normal forms

Vitality • Proportion of sperm that are alive • ;,58% live sperm

Seminal fructose • Amount of fructose per ejaculate • ;,13 umol/ejaculate

pH • pH of the ejaculate • ;,7.2
Source:CooperTG,et al. WHOreferencevaluesforhumansemencharacteristics.
2010

447
 B. Vasogram
0 Will evaluate ductal system in the absence of fructose in the ejaculate, as in:
• Seminal vesicle aplasia
• Vas deferens aplasia

C. Testicular Biopsy
0 Will distinguish obstructive azoospermia from the following non-obstructive causes:
• Sertoli only cells
• Peritubular fibrosis
• Germinal hypoplasia

II. MANAGEMENTOF MALE FACTORINFERTILITY

FACTOR I REMARKS
• Suggested mechanisms on how leukocytospermia causes infertility:
0 Direct damage to sperm & its function
Leukocytospermia 0 Increases reactive oxygen species (ROS)
• Men with leukocytes in their semen should not be offered
antibiotics unless there is an identified infection
• Decreases testicular volume, impairs sperm quality & Leydig cell function
• Cause progressive testicular damage over time
Varicocoeles
• Repair only indicated for men with palpable varicocoeles and
abnormal semen parameters
Source:NICE;2004
Tayloret al. SperoffsClinicalGynecologicEndocrinology
and Infertility,
2019

INTRAUTERINE INSEMINATION
• Concentrated washed sperm preparation is deposited directly into the uterine cavity
around the time of ovulation
• Rationale: bypass cervical factor; remove seminal plasma; initiate sperm capacitation;
increase conception rates by increasing the density of motile sperm with a high
proportion of normal forms that will reach the site of fertilization
• Requires at least one healthy fallopian tube

Indications:
• Male factor infertility • Mild endometriosis
• Unexplained infertility • Cervical factor infertility

ASSISTED REPRODUCTIVE TECHNIQUES

• Encompass all techniques involving direct manipulation of oocytes outside of the body
• Any treatment or procedure that involves the in vitro handling of human oocytes and
sperm or embryos for the purpose of establishing a pregnancy

Indications:
• Tubal factor infertility
0 Bilateral hydrosalpinx or distal tubal obstruction and tubal reconstruction is not possible
0 If no pregnancy one year after tubal reconstruction
• Severe endometriosis
• Severe male factor infertility
0 Severe oligospermia (total motile count (TMC] < 1 million after semen preparation)
0 Azoospermia
, Ejaculatory disorders
• Ovarian Factor
0 Ovarian failure and diminished ovarian reserve
0 Ovulatory dysfunction (PCOS, chronic anovulation)
• Unexplained infertility in patients who have tried other treatments
• Fertility preservation

448
I. SPERM COLLECTION
• Ejaculation is the usual method for semen collection
• Microsurgical sperm collection: because of the limited number of sperms collected, these
procedures are reserved only for planned lntracytoplasmic Sperm Inseminations (ICSls)
in relation with doing In-Vitro Fertilizations and Embryo Transfers (IVF-ETs)

A. MESA (MicroEpididymal Sperm Aspiration) for Obstructive Azoospermia

0 Involves aspiration of sperms which might have accumulated in the epididmis because
of obstruction distal to the epididymal tail

B. TESE (TEsticular Sperm Extraction) for Non-obstructive Azoospermia

0 Involves recovering sperms directly from the testis by doing a wedge resection of the
testicles and macerating the testicular tissues to free the sperms from the Sertoli cells

II. OOCYTE RETRIEVAL

• For Gamete lntrafallopian Tube Transfer (GIFT), Zygote lntrafallopian Tube Ttransfer
[ZIFT), and In-Vitro Fertilization and Embryo Transfer (!VF-ET)
• Retrieved from mature follicles through laparoscopic or ultrasound-guided aspiration
usually after ovarian stimulation

III. GAMETE INTRAFALLOPIAN TUBE TRANSFER (GIFT)

• Mature oocytes along with prepared sperms are placed into the ampullary portion of one
or both fallopian tube/s laparoscopically
• Requires at least one healthy fallopian tube
• Both oocytes & sperm are placed into the oviduct at midcycle laparoscopically
• Fertilization takes place in the ampulla of the fallopian tube

IV. ZYGOTE INTRAFALLOPIAN TUBE TRANSFER (ZIFT)

• The oocytes are fertilized in-vitro
• Fertilized oocytes at the pro-nuclei stage are placed into fallopian tubes laparoscopcally
• Requires at least one healthy fallopian tube

V. IN VITRO FERTILIZATION (!VF)

Microdrop • Microdrops of gamete preparation media with a concentration of

Technique 50,000-500,000 sperms/mL are placed over individual oocytes
Intracytoplasmic • A single viable sperm is injected directly into an oocyte in Metaphase II
Sperm Injection • Achieves the highest fertilization and pregnancy rates for both male-
(JCS!) factor and female-factor infertility

VI. EMBRYO TRANSFER (ET)

• Embryos are transcervically introduced into the uterine cavity using a flexible catheter
• Embryos delivered deep into the uterine cavity close to uterine fundus
• Embryos have been transferred successfully at any stage of development from zygote to
blastocyst, but now transfer is most commonly done during the blastocyst stage

449
 SECTION SIX
MENOPAUSE
OVERVIEW OF MENOPAUSE
• Cyclical ovulation continues for almost 40 years between menarche and menopause
• Genetically predetermined physiologic event

I. DEFINITIONOFTERMS
TERM I DEFINITION
• Permanent cessation of menstruation due to loss of ovarian
follicular activity
Menopause
• 12 months of amenorrhea after the LNMP with no attributable cause
• Body goes through changes that no longer allow her to get pregnant
• Years prior to menopause that encompass the change from normal
Perirnenopause
ovulatory cycles to cessation of menses.
(Menopausal
• Skipped periods, or longer intervals ( 40-60 days), is the hallmark of
Transition)
perimenopause
• Period of time when a woman passes from reproductive age to
non-reproductive age
Climacteric • Includes perimenopause, menopause and postmenopausal years
• Because cessation of menses is variable, and related symptoms may
occur prior, there is no precise timing to this event

II. EPIDEMIOLOGY
OF MENOPAUSE
PERIOD I TIMELINE*
Perimenopause
• Mean age: 45.1 (39 to 51 years old)
(Menopausal
• Mean duration: 5 years
Transition)
• Average age of menopause worldwide is 51 years old
Menopause • Mean age (Filipinos): 48 years old
• Age range: 44 to 56 years old
'Modernwomenare spendinga greaterportionof theirlivesaftermenopause(becauselifeexpectancyis
increasingoverthe years)

Ill. PHYSIOLOGYOF MENOPAUSE

• Due to the natural decline in the number of functioning eggs within the ovaries
• Menopause brings along with it a complex series of hormonal changes characterized with
the elevation of the gonadotrophins FSH and LH due to a negative feedback brought about
by the lack of endogenous estrogen produced by developing follicles

A. Menopausal Transition (Perimenopause)

Initial endocrinologic changes:
0

• Decreased anti-Mullerian hormone (AMH)

• Decreased ovarian inhibin B production
• Increased FSH
Estradiol does not begin to significantly diminish until ~1 year before menopause
0

B. Hormone Production After Menopause

° FSH increase 10-20x
0LH increase 3x
0Androstenedione becomes the principal steroid secreted by ovary
0Testosterone production decreases by 25%
0Sex hormone binding globulin (SHBG) decreases
0Estradiol levels markedly decline
0Androgen/estrogen ratio drastically increase
0DHEA and DHEA-Sdecrease
450
MANIFESTATIONS OF MENOPAUSE

I. OVERVIEW OF THE EFFECTS OF MENOPAUSE

• Since the estrogen affects the genitourinary tract, the skin, the blood vessels, the heart,
the brain and the bones among others, the following are the possible manifestations of its
deficiency:
SYSTEM I EFFECTS
• Hot flashes and night sweats
Vasomotor
• Headache, fatigue
• Dry skin, wrinkles due to decline in collagen content & skin thickness
• Vaginal dryness
Skin
• Urogenital symptoms (e.g., frequent urination, incontinence)
• Hair loss
• Increased total body weight and waist-to-hip ratio
Metabolic • Shift of fat distribution from a gynecoid to android type
• Decreased bone mass
• Increased risk for cardiovascular disease and stroke
Cardiovascular
• Increased total cholesterol and LDL/HDLratio
• Depression, irritability, anxiety, decreased self-esteem, mood swings
Psychological • Sleep disturbance (e.g., difficulty falling asleep, frequent awakenings)
• Cognitive changes

II. SPECIFIC MANIFESTATIONS

• Most common menopausal symptom
• Sudden sensation of heat in chest area radiating to the head & neck,
accompanied by:
, Reddening of skin
, Increase in heart rate
0 Profuse sweats (night sweats)
Hot Flashes
0 Anxiety, irritability, palpitations and panic
• May be due to the shifting of the temperature set-point at the
thermoregulatory center of the brain resulting in the narrowing of the
thermoneutral zone
• Decrease in circulating level of estrogen alters the hypothalamic
thermoregulation
• As estrogen levels decline, the lining of the vagina become thinner and
drier, smooth muscles become less elastic resulting in dyspareunia
• Menopausal women have a more alkaline vaginal pH:
, More prone to vaginal infections
0 May lead to perinea! itchiness and discomfort
Genitourinary
• Urinary tract changes:
Syndrome of
Decrease in collagen content of the structures that support the

I
0
Menopause
uterus causes pelvic relaxation that causes uterine prolapse
, Decrease in the collagen content of the endopelvic fascia causes
cytocoele and rectocoele
0 Atrophic changes in the urinary tract lining and loss of ureteral tone
causes urinary urge incontinence & frequent urinary tract infections
• A complex interaction involving several factors that culminates in
decreased interest in sex among elderly women:
Sexual , Body changes
Dysfunction , Vasomotor symptoms
0 Effects of atrophy (e.g. painful sex from dryness)
0 Decreased libido secondary to decreased testosterone levels

451
 • Osteoporosis: bone formation does not keep pace with bone resorption
Diagnosed by bone mineral density assessment by DEXA
0

• During the menopausal transition, bone loss is accelerated

Decreased
Bone resorption > bone formation
0
Bone Mass
Bone loss in itself is asymptomatic but increases the risk of fractures
0

• Loss of trabecular bone (spine)> loss of cortical bone with estrogen

deficiency
• Often aggravated by significant life-changing events that seem to
coincide with midlife like:
Marital issues
0

° Financial insecurities
Emotional
Empty nest syndrome
0
Lability
Death in the family
0

Medical problems
0

• Midlife is for many a time of personal emotional turmoil and coping

challenges brought on by fears and anxieties about getting older

MANAGEMENT OF MENOPAUSE
I. OVERVIEW OF MANAGEMENTOPTIONS
• Low dose estrogens +/- progestins
• Hormonal
• Tibolone

Drug Therapy • Selective estrogen receptor modulators (SERM)

• Non- • Bisphosphonates
Hormonal • Calcitonin
• Vitamin-D
Non- • Lifestyle • Nutrition and exercise
Pharmacologic
Therapy • Counseling • Education

• Phytoestrogens
Alternative Therapy
• Traditional medicine

II. MANAGEMENTOPTIONS FOR SPECIFICSYMPTOMS

• The severity of these symptoms varies from tolerable to debilitating
• Often transient and worst only during the perimenopause
• Treatment is better individualized and symptom-directed

SYMPTOM I OPTIONS
• Estrogen is the best therapy for the hot flash
Vasomotor • Clonidine
flashes • Selective serotonin reuptake inhibitors (SSRI) (i.e., paroxetine)
• Others: vitamin-E, black cohosh, gabapentin
Vaginal • Lubricant
atrophy • Vaginal estrogen
• Calcium and vitamin-D supplementation
Osteoporosis
• Bisphosphonates, calcitonin, tamoxifen, raloxifene
(to improve
bone density)
• Weight bearing exercise
• Reduction in smoking, caffeine, and alcohol intake
Cardiovascular • Improvement of lifestyle and diet
risk • Optimal blood pressure control

452
III. HORMONEREPLACEMENTTHERAPY (HRT)
• Most effective means of treatment of menopause
, Not given to asymptomatic women interested exclusively for cardiovascular protection or
neurocognitive protection
• Prerequisites prior to H RT:
Do clinical history, PE and labs to identify indications & contraindications
0 Recommended work-up: pelvic ultrasound, Pap smear, lipid profile, mammogram, DEXA

A. Available Regimens for HRT:

REGIMEN I REMARKS
Oral Regimens *
• CEE 0.3-0.625 mg or EV 1-2 mg daily continuously. If with uterus, add:
0 MPA 2.5 mg daily continuously or MPA 5.0 mg 12 days per 28 days,
Hormonal OR
Replacement 0 MicroP 100 mg daily continuously or MicroP 200 mg 12 days per
Therapy 28 days
• One E2/DRSP 0.5mg/0.25mg tablet or one E2/DRSP 1mg/0.5mg
tablet once daily

Contraceptive • EE/NETA 20 mcg /1 mg

Pills • EE/ LNG 20 mcg EE/0.15 mg

• Synthetic steroid with estrogenic, progestogenic and androgenic effects

• Given at 2.5 mg tablet daily continuously (same precautions as
Tibolone combined HRT)
• Preferable in post-menopausal women with vasomotor symptoms and
concomitant sexual dysfunction and/or mood disorder
Transdermal'Regimen *
• Can be administered by patch, gel, emulsion, or spray
• Ideal dose is that which allows for systemic symptom relief
Transdermal
• Presently, the preferred route of estrogen administration because
estradiol
of the lower risk of thrombotic events compared with oral estrogen
therapy
* Systemic administration (oral and transdermal regimens) of estrogen replacement
therapy, based on the symptoms, must be given at the lowest effective dose. Progesterone
must be given together with systemic estrogen if HRT is intended for menopausal women
with a uterus to prevent endometrial hyperplasia and cancer
Topical Regimens **
• 1/2 gram (estriol 1.0 mg or CEE 0.625 mg/1.0 g cream) typically daily
Estrogen
for the first two weeks; then twice a week
Cream
• Not helpful with vasomotor symptoms

Estradiol • EE 10 mcg tablet typically used daily for the first two weeks; then

I
Vaginal twice a week
Tablets • Not helpful with vasomotor symptoms

•• Topical estrogen replacement therapy (ERT) hardly reaches systemic levels. Does not
require concomitant progesterone administration. Use of topical preparations alone should
be primarily considered if hormonal treatment is solely for vulvovaginal symptoms
E2: estradiol
GEE:conjugatedequine estrogen
DRSP:drospirenone
EV:estradiolvalerate
EE: ethinylestradiol
MPA:medroxyprogestetroneacetate
NETA:norethisteroneacetate
MicroP:micronizedprogesterone
LNG:levonorgestrel
Source: InternationalMenopauseSociety,2016
PSCMCPG on Care for the MenopausalWoman,2017

453
 B. Benefits ofHRT
0 HRT will address and minimize symptoms mostly linked to the vasomotor and
atrophic effects of menopause
• Proven benefit for: vasomotor symptoms, genitourinary syndrome of menopause,
bone health
• Cardiovascular benefits when given within 10 years of the onset of menopause, but
must not be given exclusively for the prevention of coronary heart disease
• Inconclusive benefit for dementia
0 The benefits of HRT may be maximized while minimizing its deleterious effects by
giving the hormones:
• At the lowest effective dose
• Early, when it is expected to be most helpful
• No longer than necessary
• Based on the symptom of concern

C. Contraindications to HRT
° Current, past, suspected breast cancer
° Known or suspected estrogen dependent malignant tumors (e.g., endometrial cancer)
0 Undiagnosed genital bleeding
0 Untreated endometrial hyperplasia
0 History of venous thromboembolism
0 History of arterial thromboembolism
0 Untreated hypertension
0 Active liver disease
0 Hypersensitivity to active substances or HRT excipients
0 Porphyria cutanea tarda

Source:PracticalRecommendations
for HRTfor the Peri-and Postmenopause,
2004.28

IV. ALTERNATIVES TO HORMONAL REPLACEMENT THERAPY

A. Non-Hormonal Medical Therapy
0 If risk benefit ratio is not in favor of the good that HRT will provide against the bad,
non-hormonal medications may be resorted to
0 There is no strong evidence to suggest that they are as effective as estrogen in
addressing vasomotor symptoms
FOR HOT FLASHES I FOR BONE DENSITY
• Vitamin E • Calcium
• Black cohosh • Raloxifene
• SSRI • Tamoxifen
• Clonidine • Calcitonin
• Gabapentin • Bisphosphonates

B. Lifestyle Modification
0 Efforts to modify the climacteric's lifestyle and environment may be resorted to when
medical options are contraindicated
General • Age-appropriate make-over and preference for cooler clothing
Modifications • Environmental modification
Diet • Avoiding alcohol, caffeine and spicy food
• Weight-bearing exercises
Activities
• Relaxation techniques
• Optimize foreplay
Sexual • Use water-based lubricants
Modifications • Engage in non-coital activities with partner
• Regular sexual activity to maintain vaginal health

454
~4 iiii·l~►i#ii~---
I_ - - FERTILITY PRESERVATIO_N___ ~---

OVERVIEW OF FERTILITY PRESERVATION

• Due to the improvement of oncologic therapy, there is an increase in cure rates of
some hematologic cancers and solid tumors
• With the progress in the science of assisted reproductive technology, fertility preserving
procedures are now made possible which may be availed of prior to initiating cancer
therapy

GONADOTOXICITY OF CANCER THERAPY

• Cancer therapy, while lifesaving, may pose a risk to fertility
• In the ovaries:
Accelerated recruitment of primordial follicles
0 Destruction of follicles (apoptosis)
0 Decrease ovarian reserves
• In the testicles:
Inflict damage on the cellular DNA of developing spermatogonia
° Cause death of spermatogonial stem cells

Gonadotoxicity of Different Cancer Therapies

HIGH RISK I 1NTERMEDIATE RISK I LOW OR NO RISK
• Total body irradiation • Cisplatin • Methotrexate
• High dose • Carboplatin • 5-fluorouracil
cyclophosphamide • Doxorubicin • Vincristine
• Chlorambucil • Vinblastine
• Melphalan • Bleomycin
• Busulfan • Actinomycin
• Nitrogen mustard
• Procarbazine

MANAGEMENT OPTIONS
I. OVERVIEWOF MANAGEMENT

FOR MALES I FOR FEMALES

• Sperm cryopreservation • Embryo cryopreservation
• Testicular tissue cryopreservation and • Oocyte cryopreservation
transplantation • Ovarian tissue cryopreservation and
transplantation

455
II. BRIEF DESCRIPTIONOF EACHMETHOD
METHOD I REMARKS
Sperm • Involves freezing and banking sperms collected through
cryopreservation ejaculation, epidydimal aspiration, or testicular sperm extraction
• Requires time for ovarian stimulation and harvesting of ova prior
to cancer treatment
Embryo
• Ideal for married patients
cryopreservation
• Harvested eggs are fertilized & frozen for transfer after cancer
treatment
• Requires time for ovarian stimulation and harvesting of ova prior
Oocyte to cancer treatment
cryopreservation • An option for female patients without partners because sperms
are not needed
Ovarian tissue • Ovaries cryopreserved or ovarian cortex frozen in thin slices
cryopreservation • Potential option for prepubertal girls; presently experimental
Testicular tissue • Freezing of testicular tissue for re-implantation after treatment
cryopreservation • Potential option for prepubertal boys; presently experimental
• For hysterectomized women in countries where surrogacy is
restricted or prohibited
Uterine • Has already resulted in livebirth with:
transplantation 0 Immunosuppressant therapy all throughout pregnancy
0 Assisted reproductive technology
° CS-hysterectomy after completion of family size

APPROACH IN THE MANAGEMENT

I. SECURINGCONSENT
• Adult patients: secure informed consent
• Adolescent patients: require a surrogate decision maker (assent)

II. TREATMENT PLANNING

• Due to the experimental nature of some modes of fertility preservation, patient's
treatment plan should be reviewed and approved by institutional review boards.
• Fertility preservation options depend on the patient's:
0 Age/civil status/partner status
0 Diagnosis/prognosis
0 Type of cancer treatment/need for surgery
0 Need for ovarian stimulation
0 Time available for fertility preservation procedures prior to cancer treatment
• Consider:
0 Embryo cryopreservation for post pubertal women with partners
0 Oocyte cryopreservation for post pubertal women without partners
Ovarian tissue cryopreservation for prepubertal girls with immature HPO axis
Sperm cryopreservation for post pubertal males
Testicular tissue cryopreservation for pre pubertal males

III. MULTIDISCIPLINARYAPPROACH
• Ideally, the decision about who is a candidate for fertility preservation should be
rendered by a team including the following: oncologist, ART specialist, pathologist,
psychologist, and bioethicist
• The oncologist plays a special role in:
Prognosticating the long-term survival of the patient
0 Informing patients about the risk that their cancer treatment will permanently impair
fertility
Referring to psychosocial providers
0 Referring interested patients to reproductive specialist
4S6
ASCORecommendations on Fertility Preservation in People Treated for Cancer

Assessment of risk for infertility

Communicate the risk with patients
I I

Patient at risk for treatment induced infertility AND

Patient interested in fertility preservation options
I I

Refer to specialist with expertise in

fertility preservation methods
I I
i l
Eligible for proven fertility lnvestigational Fertility Preservation
preservation methods: Technique

Males: Sperm Cryopreservation . Cryopreservation of testicular

and ovarian tissue
.
..
Female:
Embryo Cryopreservation
Ovarian/Testicular Suppression
using GnRH
Conservative Gynecologic Surgery
.
. Oocyte Cryopreservation
Oophoropexy

Source:ASCO,2018

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86. Philippine Society of Reproductive Endocrinology and Infertility. Clinical Practice Guidelines in the Management of
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87. Philippine Society for Reproductive Medicine. Clinical Practice Guidelines on Endometriosis, 2014 •
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460
FAMILY
PLANNING
 SECTION ONE
OVERVIEW OF FAMILY PLANNING

FAMILY PLANNING
• With the ever-increasing population, there is definitely a need for us to find ways of
sustaining its growth
• With the limited resources available to man, controlling the population growth may be
more feasible
• Contraception remains to be a viable option
• There are two major types: temporary and permanent planning methods

I. TEMPORARYPLANNINGMETHODS
METHOD DESCRIPTION

Natural Family Planning Methods

Sexual abstinence • Abstaining from vaginal intercourse
Coitus • Also known as withdrawal method
interruptus • Removal of the penis from the vaginal canal prior to ejaculation
• Pe1iodic abstinence from sexual intercourse during the fertile window
• Includes
0 Cervical mucus method (Billing method)
Fertility 0 Basal body temperature method
awareness 0 Symptothermal method
methods 0 TwoDay Method®
0 Calendar rhythm method
0 Standard days method
0 Lactation amenorrhea method
Hormonal Methods
• Combined hormonal contraceptives that contain estrogen and
Combined oral
progesterone
contraceptives
• COCsare also known as "the pill", oral contraceptive pills (OCP), or
(COC)
oral contraceptives (OC)

• Hormonal contraceptives that only contain progestogens

Progestin-only
•Maybe given via oral contraceptive pills (mini-pills), injectable
contraceptives
progestins (DMPA),or etonogestrel implants (ENG)

Intrauterine Devices (IUD) ~

• Non hormone containing contraceptive device inserted through the

Copper IUD
cervix and positioned into the uterine cavity
Levonorgestrel-
• Hormone containing intrauterine device that mediates its
containing JU
contraceptive action via the release of levonorgestrel
system (LNG-IUS)
,;
Barrier Methods

■
• Latex or polyurethane sheath that forms a physical barrier and keeps
Condom sperm out of the vagina
• For males and females
• Thin, dome-shaped membrane of latex rubber or silicone that creates
Diaphragm a mechanical barrier between the vagina and the cervix
• Should be used with spermicides
Spermicidal • Immobilizes or kills sperm on contact by destroying the sperm cell
foam or gel membrane
463
II. PERMANENTPLANNINGMETHODS
METHOD I DESCRIPTION
• Occlusion, transection, or removal of the fallopian tubes; prevents the egg
Female
from reaching the uterus and also keeps the sperm from reaching the egg
sterilization
• Includes bilateral tubal ligation (BTL), bilateral salpingectomy
Male
• Occlusion of the lumen of the vas deferens that prohibits sperm from
sterilization
(vasectomy) passing into the ejaculate

COMPARING EFFECTIVENESS OF FAMILY PLANNING METHODS

Unintended I How to
TIER
I METHOD
I Pr~g~ancy
wothon 1"
Make your
Method Most
year of use Effective?

Subdermal implants I· 0.1%

(Etonogestrel implant)

Intrauterine systems

T
(Levonorgestrel 0.1-0.4%
intrauterine system) • After the
procedure,
Intrauterine device little or
0.8%
(copper IUD) nothing
to do or
1 remember
HIGHLY
EFFECTIVE • For
Vasectomy 0.15% vasectomy,
use another
method for
the first 3
months

Bilateral tubal ligation

(BTL)
\~ 0.5%

~
Injectable suspensions • Get repeat
(e.g., Depo-
Medroxyprogesterone
/(1) 4%
injections.
every 3
acetate (DMPA]) months

• Take a pill
~
Oral contraceptives
2 7% on time each
pills (OCP)
VERY day
EFFECTIVE • Replace
Contraceptive patch
0 7%
weeklyx 3
weeks per
month
• Keep ring in
Vaginal ring
\) 7%
place for 3
weeks per
month
464
 Unintended I How to
TIER
I METHOD
IPregnancy
wothon 1"
year of use
Make your
Method Most
Effective?

Diaphragm

0 . .
17%

Male condom 13%

Female condom 21%

• Use correctly
every time
you have sex
3
Withdrawal method 22%
EFFECTIVE

Spermicides 21%

• Abstain or use
Fertility awareness-
23% condoms on
based methods
fertile days

Tier1: <1 pregnancy

per100womenin thefirstyearof use

■
Tier2: 4-7pregnancies
per100womenin thefirstyearof use
Tier3: >13pregnancies
per100womenin thefirstyearof use

Long-acting reversible
contraceptives (LARCS},likethe injectables,
implants,andthe intrauterine
devices,areless
user-dependent andarethereforemorereliableevenwithtypicaluse.Requiringlessconscious effort,compliance
is
easierfor the userthusfacilitatingproperusage
Sources:TrussellJ, et al. Contraceptive
technology;
2018
WHO.FamilyPlanning:
A GlobalHandbook for Providers;
2018

465
MEDICAL ELIGIBILITY
• Reversible contraceptives are designed for the protracted use of preventing pregnancies
• The risk:benefit ratio for contraceptives must be individually ascertained, especially for
women with medical co-morbidities
• The World Health Organization (WHO) through its Medical Eligibility Criteria (MEC)
provides recommendations for safe prescription of contraception for all medical
conditions a potential user might possibly have
• Based on the latest clinical and epidemiological data, depending on the medical condition,
the WHO MECcategorizes each type of medical contraceptive as follows:

CATEGORY I WITH CLINICAL JUDGMENT

I
WITH LIMITED
CLINICAL JUDGMENT

1 • Use method in any circumstance Yes

(Use the method)
2 • Generally use the method
• Use of method not usually recommended
3 unless other more appropriate methods No
are not available or not acceptable (Do not use the method)

4 • Method not to be used

Where resources for clinical judgment are available, the medical contraceptive may be
categorized WHO MEC 1 to 4. For example, for ischemic heart disease:
ISCHEMIC HEART DISEASE

Combined 0CP 4 • Method not to be used

Progestrin-only pills 2 • Generally use the method
• Use of method not usually recommended
DMPA injectables 3 unless other more appropriate methods are not
available or not acceptable
ENG implant 2 • Generally use the method
Copper IUD 1 • Use method in any circumstances

Where resources for clinical judgment are limited, such as in community-based services,
the four-category classification framework can be simplified into two categories ("Yes"
if WHO MEC 1 or 2 and "No" if WHO MEC3 or 4). For example, for ischemic heart disease:
ISCHEMIC HEART DISEASE

Combined OCP 4 • No, do not use method

Progestrin-only pills 2 • Yes, use the method
DMPA injectables 3 • No, do not use method
ENG implant 2 • Yes, use the method
Copper IUD 1 • Yes, use the method

I The WHOMECdocument,wheel,and app may be downloadedat

~ ·•~th.ed,1,¢11\lOIS
}_,4.1,]M~d1calelig1b1lity1•
, rnteria for
contraceptiveuse ;
I https://www.who.int/publ ications/ i/i tem/9789 2415 4915 8
Source:WHO.Medicaleligibilityfor contraceptive
use;2015.
466
 SECTION TWO
NATURAL FAMILY PLANNING METHODS

NATURAL(FERTILITYAWARENESS-BASED) METHODS
• The use of natural means of avoiding pregnancy may be safe, but are the least reliable of
the options
• Involves identifying the fertile days of the menstrual cycle using a combination of cycle
length and manifestations of ovulation (e.g., change in cervical secretion) and then
avoiding sexual intercourse on those days

I. RATIONALEFOR PERIODICABSTINENCEIS BASED ON THREE ASSUMPTIONS:

• The human ovum is capable of being fertilized between 12-24 hours after ovulation
• Spermatozoa retain their fertilizing ability for only about 48-72 hours a~er coitus
• Ovulation usually occurs 12-16 days (14 ± 2 days) before the onset of the subsequent menses
Identifying the Six-Day Fertile Window is Critical - the probability of pregnancy is:
PROBABILITY OF PREGNANCY
PERIOD
I (from unprotected intercourse)
5 days before ovulation 4%
2 days before ovulation 25-28%
During 24 hours after ovulation 8-10%
Remainder of the cycle 0%

II. PATIENT SELECTIONFOR NATURAL FAMILYPLANNINGMETHODS

A. Candidates
o Women who do not desire other contraceptive methods
o Women who can comply with natural method requirements
o Women who will abstain from sexual intercourse on fertile days

8. Relative Contraindications
o Irregular cycles
o Inability to track physiologic changes
o Lack of supportive partner

Ill. METHODS
• Sexual abstinence
• Coitus interruptus
• Fertility awareness methods

SEXUALABSTINENCE
• Avoidance of vaginal intercourse
• Simple and 100% effective with perfect use
• Easier said than done
• Needs strong discipline and an even stronger will power and determination

-=-C-=-0..:....:IT'--=U;..;:S:....:l:...:.NT..:...;E=-:Rc...:.:Rc...:.cU::..:P-'T:....:U:....:S:....._
_______________ _
• "Withdrawal method" or the practice of withdrawing the penis from the vaginal canal
before ejaculation
• 74% effective at best
• Many males do not know when or may not have the will power to pull out in time
• Small amount of pre-ejaculate on erect penis for lubrication can still expose to infections
or a possible pregnancy

467
FERTILITY AWARENESS-BASED METHODS
• A technique of identifying fertile and infertile phases in a woman's menstrual cycle by
observing signs and symptoms
• Least effective even with perfect use
• Complex and tedious
• Needs strong motivation
Needs cooperation of the partner
• Ovulation may occur irregularly

I. CERVICALMUCUSMETHOD (BILLINGMETHOD)
• Based on the observation of changes in the cervical mucus and sensation of wetness and
dryness in relation with day of the menstrual cycle
• Near ovulation, mucus production increases and it becomes thinner in consistency
• Fertile period begins when watery mucus is noted and sensation of wetness is felt after
menses and ends 3 days after the last day of slippery mucus
• Refrain from vaginal intercourse once presence of clear, wet, and slippery mucus
secretion is observed until the 4th day after her peak day of wetness

Billing Method: insert finger into vagina and get some mucus & stretch it using the thumb
and middle/index finger. The following may be observed:
• For thin mucus (predominantly estrogen), • For thick & viscid mucus (predominantly
do not have sexual contact during this time progestin), may have unprotected sexual
(woman is fertile) contact

II. BASAL BODYTEMPERATURE (BBT) METHOD

The basal body temperature (BBT) is the lowest temperature of a healthy person upon
waking up after at least 3 hours of uninterrupted sleep
Basal body temperature rises under the influence of progesterone produced by corpus
luteum (body temperature of the woman rises 0.2 to 0.5°C around the time of ovulation)
After ovulation, there is a sustained rise of temperature
Relies on slight changes: sustained 0.5°C increase in the morning BBT which occurs just
before ovulation
Abstain from sexual contact from first day of menses until 3 days after sustained temperature
rise of 0.2 to 0.5°C; after which, may have coitus up until the next resumption of menses

1:::=-•·.··~···~
----- UNSAFEPERIOD ------ SAFEPERIOD--
Ovulation occurs

Day of menstrual cycle

III. TWODAYMETHOD®
• Helps women determine whether they are fertile at any given day
• Based on the presence or absence of cervical secretions
• If a woman notices secretions, the couple should refrain from vaginal intercourse on that
day and the day after

468
I~SYMPTOTHERMALMETHOD
• Combination of cervical mucus and BBT methods and observation of certain symptoms
• Changes in cervical mucus ( onset of fertile period]
• Changes in BBT (end of fertile period)
• Refrain from vaginal intercourse when the woman senses cervical secretions, until both
the 4 th day after peak cervical secretions and the 3rd full day after the rise in BBT
• lfthere is disparity in the application of rules of both methods, the more conservative
rule will be followed

V. CALENDARRHYTHM METHOD
• Requires recording of the length of 6 previous menstrual cycles

Formula:
• Shortest cycle minus 18 is the first day of fertile period
• Longest cycle minus 11 is the last day of fertile period
• Do not have sexual contact during the computed fertile period
Example: A patient's shortest cycle is 28 days and her longest cycle is 32 days
• 28 - 18 = 10; Day 10 is the first day of fertile period
• 32 - 11 = 21; Day 21 is the last day offertile period
• Therefore, avoid unprotected coitus from Days 10 to 21

VI. STANDARD DAYSMETHOD

• Calendar-based method that determines fertile days using two sets of probabilities:
o Probability of pregnancy with respect to ovulation
o Probability that ovulation occurs near the midpoint of the cycle
• Avoid unprotected intercourse from day 8 through day 19 of the cycle (12 days]
• A visual tool may be used for this method such as Cycle Beads® (string of 32 color-coded
beads) which is a string of beads helps woman identify fertile days of cycle

If bleeding occurs after reaching

the last brown bead, the cycle is
DAY1
longer than 32 days.
On the first day of menstrual bleeding, move
the rubber ring to the red bead
If bleeding occurs before reaching
the dark brown bead, the cycle is
shorter than 26 days. ! Move the ring to the next bead
~-

Gray beads - pregnancyis unlikely;

may have unprotectedsex
White beads - pregnancy is likely;
should avoid/have protected sex

• Should be used only by women with 26-32 days cycle

• Woman moves a rubber ring over one bead every day to track where she is in her menstrual cycle
• Woman avoids intercourse when the rubber ring is on a white bead (days 8 through 19)
representing a fertile day
Source:JenningsV. Uptodate;2021
DOH.The PhilippineClinicalStandardsManualon FamilyPlanning;2017
I
..

VII. LACTATIONAMENORRHEAMETHOD (LAM) '

• The woman is 95% protected from pregnancy for the first 6 months when she is purely
breastfeeding (continuous suckling induces nerve impulses to the hypothalamus)
• Prolactin inhibits gonadotropin pulsatility
• Requirements:
o Mother is within the first 6 months after delivery
o Fully or nearly fully breastfeeding (every 4 hours in the day, every 6 hours at night)
o No resumption of menses yet

469
 SECTION THREE
HORMONAL CONTRACEPTION
OVERVIEW OF HORMONAL CONTRACEPTION
• Use is independent of sexual intercourse (does not interfere)
• Can be carried out without partner's knowledge
• The choice between combined oral contraceptives (COCs) and progestin-only
contraceptives is the biggest issue that needs to be hurdled

COMBINED HORMONAL CONTRACEPTIVES

• Prevents ovulation by suppression of the hypothalamic gonadotrophin-releasing factors,
thereby preventing pituitary secretion of FSH and LH
• May be given via pills, patches, rings, and injectables
• Contain an estrogen component and one of different progestins:

Advantages and Disadvantages of Combined Hormonal Contraceptives

ADVANTAGES I DISADVANTAGES
• Widely available and safe • Narrow margin for error (if used
• Easy to use incorrectly /inconsistently, effectiveness is
• Non-contraceptive benefits: lowered)
o Increased bone density • Mild headaches
o Reduced menstrual blood loss & anemia • Slight weight gain, depending on progestin
o Decreased risk of ectopic pregnancy component
o Improved dysmenorrhea • May increase risk of breast cancer** and
o Fewer premenstrual complaints cervical cancer***
o Decreased risk of endometrial &
ovarian cancer*
o Reduction in various benign breast
diseases
o Inhibit progression of hirsutism
o Improvement of acne
o Prevention of atherogenesis
o Decreased incidence and severity of
acute salpingitis
o Improvement in rheumatoid arthritis
'Use of OCP reduces endometrialcancer risk by suppressing endometrialcell proliferation& ovarian cancer riskby
reducingthe numberof ovulationsin a woman's lifetime,decreasing epithelialdamage to the ovaries.

"The slightincrease in breast cancer risk is associated withthe hormonalcontent of OCPS.

'"Increase in cervicalcancer riskis associated withthe change of the susceptibilityof cervicalcells to persistent
infectionwithhigh-riskHPVtypes

Hormone Components
HORMONE I REMARKS
• Most combined oral contraceptives (COC) contain ethinyl estradiol as
estrogen component with an average dose of20-35 mcg (i.e., low dose)
Estrogen • Creates a negative feedback mechanism to prevent follicular
development, which is necessary for ovulation
• P,·events follicle maturation by suppressing FSH release

• Examples include levonorgestrel, desogestrel, norethisterone acetate,

drospirenone, cyproterone acetate, gestodene
Progestin
• Prevents ovulation by suppressing LH surge
• Thickens cervical mucus (thereby retarding sperm passage)
Source: DOH.The PhilippineClinicalStandards Manualon FamilyPlanning;2017
470
I. COMBINEDORALCONTRACEPTIVE(COC)PILLS
• COCs are pills that contain low doses of two hormones (estrogen and progestin)
• Main contraceptive efficacy is suppression of ovulation by inhibition of GnRH from
hypothalamus, LH, & FSH and disruption of the mid-cycle LH surge

A. Proper Use of COC*

• 21 pills: 21 active tablets taken every day followed by 7 pill-free
days (e.g. 30 mcg EE+ 0.15 mg LNG)
• 24 pills: 24 active tablets taken every day followed by 4 pill-free
MonthlyCOC
days (e.g. 20 mcg EE+ 0.15 mg LNG)
• 26 pills: 26 active tablets taken every day followed by 2 pill-free
days (e.g. 1-3 mg EV+ 2-3 mg DNG (multiphasic)

Extended cycle • Active pills are taken for 12 weeks followed by a one-week pill-free
preparations period for withdrawal bleeding ( e.g. 30 mcg EE+ 0.15 mg LNG)
Continuous COC • Active pills taken for 365 days a year (e.g. 20 mcg EE + 0.09 mg LNG)
EE:ethinylestradiol EV:estradiolvalerate
LNG:levonorgestrel DNG:dienogest

'Some brands comewithreminderpillsof a differentcolor.The reminderpillsdo not containhormonesand are

there onlyto remindthe user to take a pilleveryday for compliance.Takinga placeboon the hormone-freedays
wouldmean there are no pill-freedays.

1. How to Take COCs

• Take one pill regularly, preferably at the same time every day
• Start on day 1 of menses or within the first 5 days of the menstrual period.
• If certain not to be pregnant, COCs can be started anytime (i.e., quick start method)
but a back-up method (e.g., condom, abstinence) is required for 7 days if started after
the 7th day of menses
• Start again as scheduled

2. What To Do In Case Of Missed Pills?

• Take the missed pill and the pill due for that day,
1 pill missed or new
then continue taking the rest as scheduled.
pack started 1 day late
• No back-up required

2 pills missed in a row
or new pack started 2
days late
3 pills missed in a
row in the 1st and
2nd week or new pack
started 3 days late
3 pills missed in a row
in the 3rd week
• Take the last missed pill and the pill due for the day,
then continue taking the rest as scheduled.
• No back-up required
• Take the last missed pill and the pill due for the day,
then continue taking the rest as scheduled.
• Use back up for the next 7 days
• If with intercourse in the past 5 day, may use
emergency contraception
• Discard current pack and start new pack right away
• Use back-up method for the next 7 days
•ff with intercourse in the past 5 days, may use
emergency contraception

I
471
 B. Safety
o COCsdo not disrupt an existing pregnancy
o COCs do not cause birth defects and will not harm the fetus even if the woman
becomes pregnant while taking the pills or accidentally starts the pill when she is
already pregnant
ABSOLUTE CONTRAINDICATIONS I RELATIVE CONTRAINDICATIONS
• History of vascular disease • Smokers (<35 years old)
• Systemic diseases affecting vascular • Migraines
system • Undiagnosed cause of amenorrhea
• Smokers >10 cigarette sticks per day • Depression
• Uncontrolled hypertension • Prolactin-secreting macroadenomas
• Existing breast and endometrial cancer
• Undiagnosed uterine bleeding
• Elevated triglycerides
• Pregnancy
• Functional heart disease
• Active liver disease

C. Other Things to Remember:

o Drug interaction: effectiveness of COCs is reduced with rifampicin, phenytoin,
phenobarbital, carbamazepine, primidone and ethosuximide
o Side effects: spotting, amenorrhea, nausea, breast tenderness, headaches and possibly
depression
o Return to fertility: no delay of return to fertility after COCsare discontinued
o Risk for thrombosis: while the absolute risk for thrombosis in COCusers is only 0.05%
per year, this is a 3-5x increase from baseline (they affect blood clotting by increasing
activity of coagulation factors VII & X and plasminogen and decreasing activity of
antithrombin Ill, the inhibitor or coagulation)
o Risk for thrombosis is less than that of pregnancy

II. COMBINED INJECTABLE CONTRACEPTIVES

• Combined injectable contraceptives (CIC) are monthly injectable preparations that
contain a short-acting natural estrogen and a long-acting progestogen
• Once given intramuscularly (IM), these hormones are slowly released for 28-30 days
• Some preparations available:
o 25 mg depot-medroxyprogesterone acetate+ 5 mg estradiol cypionate IM once a month
o SO mg norethindrone enanthate and 5 mg estradiol valerate IM once a month

DOH.The PhilippineClinicalStandardsManualon FamilyPlanning;2017

III. OTHER DELIVERY SYSTEMS

CONTRACEPTIVE
I TRANSDERMAL PATCH
I VAGINAL RING
• Medicated adhesive
Description patches containing EE and
norelgestromin
• 20 mcg EEand 150-mcg
Dose
norelgestromin per 24 hours
• One patch weekly for 3 weeks
Administration
• Followedby patch-free week
Availability • Not available locally
472
CONTRACEPTIVE
• Sustained-release delivery system in
the form of a flexible plastic ring
• Produces a consistent concentration
of the circulating contraceptive
hormones that prevent the daily
fluctuations associated with the use
of COCs
• 15 mcg EE and 120 mcg etonogestrel
per 24 hours
• One ring every 3 weeks
• Followed by ring-free week
• Not available locally
PROGESTIN-ONLY CONTRACEPTIVES
• Contain only the hormone progestin
• Examples include progestin-only pills (POP), injectables, subdermal implants, and
LNG-IUS(discussed under IUD)
• Mechanisms of action:
o Thickening of cervical mucus and retardation of sperm passage
o Suppresses LH, blunting the LH surge
o Since there is no estrogen, there is no suppression FSH

I. PROGESTIN-ONLY ORAL CONTRACEPTIVE PILLS (POP)

• Compared to combined OCP,progestin-only pills (POP) have a:
o Higher likelihood of escape ovulation
o Higher pregnancy rate
o Higher incidence of ectopic pregnancy
• Effectiveness depends more on alteration in cervical mucus and prevention of ovulation

A. Doses/Preparations (both are available in 28-tablet packages)

o Lynestrenol 0.5 mg
o Desogestrel 75 mcg

B. Administration
o Should be taken at the same time every day ( or at least within 3 hours of usual
schedule) with no break between packs of pills; If taken 4 hours late, use of back-up
method ( e.g., condom, abstinence) for the next 48 hours

C. Advantages and Disadvantages

ADVANTAGES
• Can be given to breastfeeding mothers as it
does not interfere with milk production
• No estrogen side effects (nausea)
• Promotes compliance in pill taking (i.e.,women
take one pill every day with no break)
• May help prevent benign breast disease,
endometrial/ovarian cancer, and pelvic
inflammatory disease
• May benefit patients with endometriosis
as progestin-only pills have been shown to
suppress endometriotic lesions
DOH.The PhilippineClinicalStandardsManualon FamilyPlanning;2017
I DISADVANTAGES
• May induce changes in menstrual
bleeding and prolongs/causes heavy
menstrual bleeding in some
• Need to be taken at the same time every
day to be an effective contraceptive
as thickening of cervical mucus from
progesterone effect only lasts ~24 hours
from last intake
• Headache, breast tenderness

II. PROGESTIN-ONLY INJECTABLES

• Contain the synthetic hormone progestin and administered via deep IM injection

1 mL of 150 mg DMPA • Given every 3 months

• IM injection on either deltoid or gluteus
3 mL of 150 mg DMPA muscle without massage
1 mL of200 mg NET-EN • Given every 2 months
DMPA:depotmedroxyprogesterone
acetate ■
.__N_ET_-E_N_:
n_o_re_th_is_ter_o_ne_e_na_n_th_at_e
------------------------~ • .'
DOH.The PhilippineClinicalStandardsManualon FamilyPlanning;2017

B. Administration
o Initial injection should be given within the first 5 days of menses
o If certain not to be pregnant, the patient can be injected the initial dose at any time
during the menstrual cycle but a backup contraceptive method is required for 7 days if
given after the 7th day of menses.
o Return of fertility after 6 months to 1 year from last dose of DMPA
473
 C. Side Effects
o Irregular bleeding patterns ("breakthrough bleeding")
o Weight changes
o Headaches
o Mood changes
o Bone Loss

D. Non-Contraceptive Health Benefits

o Reduces the risk of developing iron deficiency anemia and PIO
o Reduces the risk of endometrial cancer
o Reduces the incidence of primary dysmenorrhea, symptoms of endometriosis,
ovulation pain, and functional ovarian cysts

III. ETONOGESTREL (SUBDERMAL) IMPLANT

• Thin, pliable progestin-containing cylinder that is implanted subdermally in the inner
upper arm
• Provides contraception for 3 years and then replaced at the same site or in the opposite arm
• Extremely effective, and is easy to insert and remove
• Does not result in a decrease of bone mineral density

A. Dose
o The initial serum concentration of etonogestrel (ENG) is about 800 pg/mL, decreasing
to 150 pg/mL by the end of the third year of use
o The required level to inhibit ovulation is ~90 pg/mL and implant is meant for only 3
years of use

B. Administration
o Ideally inserted within 5 days of menses
o If certain not to be pregnant, the implant may be placed at any time during the
menstrual cycle but a backup contraceptive method is required for 7 days if given after
the 7th day of menses.

C. Side Effects and Non-Contraceptive Health Benefits

o Similar to progestin-only injectables
o May also induce scarring at the implantation site

Source:ErkkolaR,et al.ActaObstetricia;
2005

474
 SECTION FOUR
INTRAUTERINE DEVICES
OVERVIEW OF INTRAUTERINE DEVICES (IUD)
An IUD is a small plastic device inserted into a woman's uterine cavity to prevent pregnancy
• Contains copper or releases a hormone ( e.g., levonorgestrel)
• Induces a local inflammatory reaction of the endometrium, creating an environment that
is hostile to sperm so that fertilization of the ovum does not occur

TYPES OF IUD
TYPE
I MECHANISM
I REMARKS
• Intense local endometrial
• Labeled for use up to 10 years but
inflammatory response
has been proven to be effective up to
• Cellular and humoral components
12 years.
of this inflammation are
• Adverse effects: heavy menstrual
Copper IUD expressed in endometrial tissue
bleeding, may be treated with
and in fluid fillingthe uterine
antifibrinolytic agents and
cavity and fallopian tubes leading
nonsteroidal anti-inflammatory
to decreased sperm and egg
drugs.
viability
• Releases LNGdirectly into the
uterine cavity at an initial rate of
20 mcg per day followed by slow,
• Local inflammatory reaction
sustained systemic release for
Levonorgestrel- • Progestin component (thickens
5 years
containing cervical mucus, impeding sperm
• It affords hassle-free, long term
intrauterine penetration and access to the
effects similar to implants, but with
system upper genital tract)
ease of discontinuation when so
(LNG·IUS) • Blunts LH surge, prevents
decided
ovulation
• Non-contraceptive benefits: reduces
heavy menstruation, dysmenorrhea,
and endometriosis

Source:SuvisaariJ, et al. Contraception;1996

I. ADVANTAGES AND DISADVANTAGES

ADVANTAGES
• Does not interfere with sexual intercourse
• Can be used without partner's knowledge
• No systemic side effect
• One time application
• No need to worry about the next dose
• Effective for 10 years (copper IUD) or 5
years (LNG-IUS)
I DISADVANTAGES
• Inserted by a trained provider
• Uterine perforations can occur
• Uterine spasms
• Menstrual irregularities
• Expulsion
• Risk for PIO
• May not be protective against ectopic
pregnancies

■
II. TIMING OF INSERTION
• The IUD can be safely inserted in any of the following scenarios:
o On any day of the cycle provided the woman is not pregnant
o During menstruation
o Immediately post-abortion
o Immediately postpartum (vaginal or Cesarean section delivery)
• Immediate postpartum insertion carries a higher risk of IUD expulsion, particularly in the
case of an LNG-IUS following vaginal delivery
, Postpartum IUD insertion is usually not done >48 hours to 4 weeks post-partum because of the
higher risk of IUDexpulsion compared to immediate post-partum and interval IUD insertion

475
III. COMPLICATIONS OF IUD
COMPLICATION
I DESCRIPTION
I MANAGEMENT

• Prolonged bleeding: >8 days • Rule out non-gynecologic causes or

Prolonged/heavy • Heavy bleeding: twice as
bleeding long or twice as much as
the usual
• Common within first 3-6
Cramping months of IUD use
• Resolves
• Pelvic infection may occur
when insertion is performed
under unsanitary conditions
Pelvic
or when IUDis inserted in the
inflammatory
presence of an undiagnosed
disease
infection
• May present with discharge,
pain, bleeding, chills, fever
Pregnancy with • Ectopic pregnancy must be
IUD ruled out (life-threatening)
• If string is not visible during
checkup and device is not
Missing string
found inside the uterus, the
IUDmay have been expelled
i • Confirm the location through
• If the IUD is identified to be
Displacement
outside the uterine cavity
• Rare and usually occurs at
the time of insertion
Uterine • Manifestations: pain during
perforation insertion, loss ofresistance
to upward pressure, signs of
hemorrhage
DOH.ThePhilippineClinicalStandardsManualon FamilyPlanning;2017
other conditions unrelated to IUD
• NSAIDs,tranexamic acid, iron
supplementation if with anemia
• Mild cramping: reassurance and pain
relievers
• Severe, persistent cramping: rule out
partially expelled IUD or infection, or
may remove IUD
• Asymptomatic PID: IUD should not
be removed
• Significant pelvic infection: treat with
long-term antibiotics and remove
the IUD
• IUDstrings visible: remove IUD
to avoid infection, miscarriage, or
premature birth
• IUDstrings not visible: locate device
with ultrasound and refer to specialist
• Perform pelvic examination,
ultrasound, or laparoscopy when
indicated
ultrasound or x-ray
• Embedded in the myometrium:
ultrasound-guided or hysteroscopic
retrieval
• Within the peritoneal cavity:
laparoscopic retrieval
• Refer to gynecologist or surgeon
• Confirm perforation with an x-ray or
ultrasound
• Stable: may be managed
conservatively
• Unstable: may proceed to diagnostic
laparoscopy or exploratory
laparotomy

IV. CONTRAINDICATIONS
• Pregnancy or suspicion of pregnancy
• Genital bleeding of unknown origin
• Known or suspected uterine or cervical malignancy
• Postpartum endometritis or infected abortion
• Acute PIO
• Testing for gonorrhea and chlamydia should be performed and IUD insertion delayed if
there is a clinical suspicion of infectious endocervicitis, or the patient has two out of three
of the following:
o Purulent vaginal discharge
o Adnexal tenderness
o Cervical motion tenderness
476
 SECTION
BARRIER METHODS
OVERVIEW OF BARRIER METHODS
• Barriers like the condom are contraindicated to those who are allergic to latex and lubricant
• Being highly user-dependent, the failure rate based on typical use may render it less than ideal.
DESCRIPTION
I ADVANTAGES
Condom (Male & Female)
• Male: latex and
polyurethane
• Female: soft, loose-fitting
polyurethane sheath with
two flexible rings
Diaphragm and Pessaries
• Thin, dome-shaped
membrane of latex rubber
or silicone with a flexible
spring molded into the
rim. The spring allows
the device to be collapsed
for insertion and then
allows expansion within
the vagina with the rim
sitting against the vaginal
wall to create a mechanical
barrier between the vagina
and the cervix
• Should be used with a
spermicide and be left in
place for at least 8 hours
after the last coital act
~ ;# ·,,2-
Spermicidal Foam o.cGel
• Active ingredient:
nanoxyl-9 (surfactant that
immobilizes or kills sperm
on contact by destroying
the sperm cell membrane)
• Spermicides need to be
placed into the vagina
before each coital act
FIVE
I DISADVANTAGES
• No systemic side effects
• User controlled
• Easily initiated and
discontinued
• Good for infrequent
contact
• Effective method for STD
prevention
• Does not interfere with
sexual intercourse if
inserted beforehand
• May be inserted 6 hours
before intercourse
• No systemic effects
• User controlled
• Easily initiated and
discontinued
• Good for infrequent
contact
p;
• Use independent of sexual
intercourse if inserted
before hand
• May be inserted 1 hour
before intercourse
• No systemic effects
• User controlled
• Easily initiated and
discontinued
• Good for infrequent
contact
477
• Use interferes with
spontaneity of sexual
intercourse
• Has false reputation of
decreased sensation,
making sex less enjoyable
to the user
• Reaction to latex
• Embarrassment in
purchasing
• Afraid to ask partner to
use it
• Needs anticipation to
insert before hand
• Interferes with
spontaneity of sexual
intercourse if not inserted
before hand
• Requires fitting by a family
planning provider
• Allergic reaction to latex/
lubricant
-
,;;
• Needs anticipation to
insert before hand
• Interferes with
■
spontaneity of sexual
intercourse if not inserted
before hand
• May produce vaginal or
penile irritation
 SECTION SIX
STERILIZATION
FEMALE STERILIZATION
• Being permanent in nature, this is only recommended for women who have completed
their desired family size or have serious contraindications to having another
pregnancy
• Patient must first be a good surgical risk without predisposition to bleeding, infection,
and anesthetic complications
• Accomplished by occlusion, transection, or removal of the fallopian tubes

ADVANTAGES
• Highly effective (0.5 pregnancies
per 100 women during first year
of use)
• Effective immediately
• Worry-free
• Does not interfere with intercourse
• Good for patient if pregnancy
would pose a serious health risk
• No long-term side effects
• No change in sexual function (no effect
on hormone production by ovaries)
I DISADVANTAGES
• Must be considered permanent (success of
reversal cannot be guaranteed)
• Patient may regret later (highest before age 30)
• Risk of surgical complications such as bleeding
and infection
• Short-term discomfort and pain following
procedure
• Requires trained physician (gynecologist or
surgeon for laparoscopy)
• Increased risk of ectopic pregnancy

I. BILATERAL TUBAL LIGATION (BTL)

• May be done via laparoscopy, mini-laparotomy, or in relation with a laparotomy for
another procedure
• Simply means, "resection of a segment of fallopian tube on both sides"

A. Methods of Tubal Resection

1. Pomeroy Method
• Most commonly used technique
• A loop of fallopian tube is ligated, and the segment of tube above the ligature is
excised
• Variations of the Pomeroy method:
POMEROY TECHNIQUE I MODIFIED POMEROY TECHNIQUE
• The middle segment of each tube is lifted • This is similarly done but with the cut
to form a loop. Absorbable ligature is used ends individually ligated as well with
to tie around the base of the loop. The loop non-absorbable sutures
above the ligation is then excised

478
 2. Other Methods
PARKLAND METHOD
• A 2-cm segment of the mid-portion
of each tube is ligated proximally and
distally with delayed absorbable sutures
• Segment between the sutures is excised
I IRVING METHOD
• After excision of a mid-segment of each
fallopian tube, the proximal part is tied to
the backside of the uterus and the distal
part is buried in the mesosalpinx

• Due to the enlarged uterus and the
consequently higher location of
the fallopian tubes, the transverse
minilaparotomy incision is made just
below the lower border of the umbilicus
• With the non-pregnant uterus barely
beyond the pelvis, the approach to the
fallopian tubes is made through a transverse
minilaparotomy incision just above the
upper border of the symphysis pubis

V
II. STERILIZATIONVIA LAPAROSCOPY
• Tubal occlusion done by using Hulka Clips or Falope Rings applied to the tubes using
specialized laparoscopic operative instruments
• Bipolar cautery and transection of the fallopian tube may also be employed

III. BILATERALSALPINGECTOMY
• In selected cases, bilateral salpingectomy may be done for surgical sterilization and at the
same time prophylaxis against some types of ovarian carcinoma
• May be performed via laparoscopy or in relation with a laparotomy for another procedure
• Couples must be advised that this procedure as a means of sterilization is permanent
with no prospects of reversal

IV. TRANSCERVICALSTERILIZATIONVIA HYSTEROSCOPY

• This is achieved with coiled microinserts placed individually in the lumen of the proximal
segments of the fallopian tubes under direct hysteroscopic visualization
• These intrafallopian devices cause (1) mechanical occlusion by the outer metallic
coil; (2) tissue overgrowth within the tubal lumen induced by the inner polyethylene
■
terephthalate (PET) fibers
• Effectivity (demonstrated through hysterosalpingogram): 96% of all insertions 3 months after
the placement procedure, 99.5% after 12 months
• Provides permanent sterilization
479
MALE STERILIZATION: VASECTOMY
• Vasectomy done on the partner may just be the safest and most effective choice of
contraception for a woman with medical problems
• Must be considered permanent (because the success of reversal cannot be guaranteed)

I.PROCEDURE
• Vas deferens of each side is blocked (tying and cutting) to prevent sperms admixing with
ejaculated semen
• lncisional vasectomy: both vas deferens are identified individually through a scrotal
incision, ligated, and transected
• No scalpel vasectomy: same as traditional vasectomy, but reaches the vas through a
puncture on the scrotum instead of through an incision
• Complete expulsion of sperms stored in the reproductive tract beyond the interrupted vas
deferens takes:
o 3 months (one cycle ofspermatogenesis)
o 20 ejaculations (to empty vas deferens distal to the vasectomy)
o Needs semen analysis to confirm azoospermia

• The vas deferens can be accessed
either through a mid line incision or
puncture made into the skin of the
scrotum
• Each vas is individually pulled through the
incision until it forms a loop
• Two non-absorbable ligatures are placed
1 cm apart
• Segment between the two ligatures is then
excised
Source:OblepiasVR,et al. Contraceptionby Surgery;1977
Adaptedfrom the illustrationby Dr.AugustoM. Manalo

II. ADVANTAGESAND DISADVANTAGES

ADVANTAGES
• Compared to vasectomy, female
sterilization is associated with:
o 20x increased complication rate
o 10 to 37x failure rate
o 3x increased cost
I DISADVANTAGES
• Major disadvantage: sterility is not
immediate
• Patient may regret later (highest before
age 31)

III. FAILURERATES OF VASECTOMY

• Failure rate (9.4 per 1000 procedures first year) due to:
o Unprotected intercourse too soon after ligation
o Incomplete occlusion of the vas deferens
o Recanalization

480
 SECTION SEVEN
EMERGENCY CONTRAGEPTION

EMERGENCY CONTRACEPTION (EC)

• Emergency contraception is an after-coitus method of preventing pregnancy following
unprotected sex
• Reasons for use include having sexual intercourse when not on any method of
contraception (52%), condom slippage or breakage (44%). Others are missed pills, rape,
and recent teratogenic exposure
• Must not be utilized as a regular method of contraception
• Methods: copper IUD,hormonal contraceptive

Source:TrussellJ. Emergency
contraception:
WHOTaskForceStudy;1998

I. MECHANISMOF ACTIONAND EFFICACY

• Delays or inhibits the release of an ovum from the ovary when taken early enough before
ovulation by preventing the LH surge
• Increases viscosity of the cervical mucus preventing sperms from reaching the ovulated egg
• Has no effects on the sperm, fallopian tubes, fertilization, implantation and corpus luteum
formation.
• If taken within 72 hours of unprotected sex, studies have shown that women given EC
have only a 1.7% to 2.6% chance of getting pregnant

K.Contraception;
Sources:Gemzel-Danielsson 2010
FinePM.AdvTher;2011
Ill. MANNEROF INTAKE
A. Oral hormonal contraceptives
o May be taken up to 5 days after unprotected vaginal intercourse, but is most effective if
taken as soon as possible within 72 hours of coitus
o For two-dose regimens, the second dose must be taken 12 hours after
o Vomiting is common with oral EC use:
• Vomiting within 2 hours of intake: repeat dose
• Vomiting after 2 hours: no need to repeat dose
• If with continuous vomiting, anti emetics may be taken
• Cannot tolerate oral doses: pills can be inserted vaginally into the posterior fornix
• For two-dose regimen, if the woman experiences nausea and/or vomits with the first
dose, she can take anti-emetics 30-60 minutes prior to intake of the second dose
o The woman should refrain from unprotected coitus after EC until onset of menses
o Advise follow-up and pregnancy test if next expected menstruation is 7 days late
o Start or re-start contraception after emergency contraception use:
• immediately (no need to wait for next menstruation)
• anytime if it is reasonably certain she is not pregnant
• while abstaining from unprotected sex or using a back-up method (e.g., condom, etc.)
for the first 7 days on the chosen contraceptive method

B. IUD
o May be inserted up to 5 days after unprotected vaginal intercourse, but is most ■
effective if inserted as soon as possible within 72 hours of coitus
o Appropriate for patients who would like to start using a highly effective, long-acting, ·:
and reversible contraceptive method
o Effectivity: >99%
Source:WHOContraecptiveFactSheet,2018

481
 PILL TYPE AND HORMONE

Dedicated ECPPr(),ducts
I
FORMULATION

- -
~ -- " -- ,-

1.5 mg LNG* 1 0
Progestin-only
0,75 mg LNG* 2 0

Ulipristal acetate 30 mg 1 0
Qra! co"ntrat;eptiv":Pills Usedfor,,_Em(!.r-oency
Contraception
0,02 mg EE+ 0,1 mg LNG 5 5
0,03 mg EE+ 0.15 mg LNG 4 4
Combined (estrogen- 0.03 mg EE+ 0.125 mg LNG 4 4
progestin) oral
contraceptives 0.05 mg EE+ 0.25 mg LNG 2 2
0.03 mg EE+ 0.5 mg norgestrel 4 4
0.05 mg EE+ 0.5 mg norgestrel 4 4

0.03 mg LNG* 50** 0

Progestin-only pills 0.0375 mg LNG* 40** 0

0.075 mg norgesterel 40** 0

• Notavailablelocally
"Many pills,butsafe

Forinformation
onbrandsof ECPSandoralcontraceptivepills,see:TheEmergency Contraception
Website(http:/
ec.princeton.edu)
andthe International
Consortium
for Emergency Contraception
(http:/www.cecinfo.org).

REFERENCES
1.Bonnar J. Coagulation effects of oral contraception. Am J Obstet Gynecol.1987;157(4 Pt 2):1042-1048. doi:10.1016/s0002-
9378[87]80129-1
2.Department of Health. The Philippine Clinical Standards Manual on Family Planning (2014 Edition), Manila, Philippines:
DOH,2014. 437 pages
3.Erkkola R, LandgrenBM. Roleofprogestins in contraception.Acta Obstetriciaet GynecologicalScandinavica,2005.Available
on line: https:/ /obgyn,onlinelibrary.wiley.com/ doi/full/10.1111/j,0001-6349,2005.00759.x
4,Fine PM. Updates on emergency contraception, Adv Ther 2011;28(2):87-90)
S.Gemzel-Danielsson K Mechanism of action of emergency contraception. Contraception 2010;82:404-409
6.Jennings V. Fertility awareness-based methods of pregnancy prevention. Uptodate. Available online https://www.uptodate.
com/contents/fertility-awareness-based-methods-of-pregnancy-prevention.Accessed on June24, 2021
7.0blepias YR, et al. Contraception by Surgery, 1977
a.PhilippineObstetricaland GynecologicalSociety in collaborationwith the PhilippineSociety for FamilyPlanning (2nd ed.),
ClinicalPracticeGuidelineson FamilyPlanning;2017
9.PhilippineSocietyof ReproductiveEndocrinologyand Infertility,Inc.QuickReferenceManualon ReproductiveEndocrinology
and Infertility: 1st ed,, Oiliman, Quezon City:, 2012
10. SuvisaariJ,Lahteenm3kiP.Detailedanalysisof menstrualbleeding patternsafterpostmenstrualand postabortalinsertionof
a copper IUD or a levonorgestrel-releasing intrauterine system. Contraception. 1996;54( 4):201
11. Sumpaico, et al (eds), Philippine Textbook of Obstetrics, 3rd ed., Quezon City: Association of Writers of the Textbooks of
Obstetrics & Gynecology, Inc., 2008.)
12. Trussell J. Emergency contraception: WHO Task Force Study. Lancet 1998;352(9135);1222-3
13. TrussellJ,AikenARA,MicksE,GuthrieKA.Efficacy;safety,and personal considerations.In:HatcherRA,Nelson AL,Trussell
J,Cwiak C, Cason P, Policar MS, Edelman A, Aiken ARA, Marrazzo J, Kowal D, eds. Contraceptive technology. 21st ed. New
York, NY:Ayer Company Publishers, Inc., 2018. Available online:https://www.cdc.gov/mmwr /pdf/rr /rr62e0614.pdf
14. World Health Organization Department of Reproductive Health and Research (WHO/RHR) and Johns Hopkins Bloomberg
School of Public Health/Center for Communication Programs (CCPJ, Knowledge for Health Project Family Planning: A
Global Handbook for Providers (2018 update), Baltimore and Geneva: CCP and WHO, 2018
15, World Health Organization. Medical eligibility for contraceptive use, 5th ed. WHO, 2015
16, Wilcox A, et al. Post-ovulatory aging of the human oocyte and embryo failure. Hum Reprod 1998; 12:394.
482
GYNECOLOGIC
ONCOLOGY
 SECTION ONE
INTRAEPITHELIAL NEOPLASIA OF THE LOWER GENITAL TRACT

ETIOPATHOGENESIS
I. PERSISTENT HIGH RISK HUMAN PAPILLOMAVIRUS
• All cases of cervical cancer are caused by persistent infection with high-risk types of
human papilloma virus (HPV)
• Double-stranded DNA virus that replicates within epithelial cells
• HPV is the most common sexually transmitted disease (STD):
0 Develop significant preinvasive disease in 3-5% of women
0 Develop invasive cancer in <l % of women
• More than 120 types with ~40 types known to infect genital tracts of men and women
• Approximately 12 types are considered high-risk, with types 16 & 18 being responsible
for 70% of cervical cancers

Clinical Manifestations and Associated HPV Types

MANIFESTATIONS* I COMMONLYDETECTABLETYPE
Slcin Lesions
-
Verrucae vulgares, verrucae palmares et plantares 1, 2, 4
Verrucae planae 3, 10
Butcher's warts 7
Squamous cell carcinoma of the finger, Bowen disease 16
Epidermodysplasia verruciformis (EV) 3,5,8
EV-squamous cell carcinomas 5,8
, M~_cosalLesions
- ~
..
·:
--- - - :'

Condylomata acuminata 6, 11
High-grade squamous intraepithelial neoplasia & 16,18
invasive carcinomas of the anogenital tract
Bowenoid papulosis, erythroplasia ofQueyrat 16
Buschke-Lowenstein tumor 6, 11
Laryngeal papillomatosis 6, 11
Heck disease 13, 32
'Otherthancervicalcancer,HPVcanalsocausecancersin theoropharynx,
anus,penis,vulva,vagina

II. PATHOGENESIS
• High-risk HPV causes neoplastic cellular changes when viral DNA becomes integrated
into the host cell genome leading to loss of repressor areas of the viral genome
• Allows expression of the viral E6 and E7 genes leading to the production of oncoproteins
resulting to inactivation of the p53 and retinoblastoma tumor suppressors ➔ cell
immortalization and rapid cell proliferation (Le. loss of apoptosis or programmed cell death)
• Majority of cases associated with infection of one or more types of HPV
• Cervical cancer develops in 15 to 20 years in women with normal immune systems vs 5 to
10 years in women with weakened immune systems (Le untreated HIV infection) ■

485
 LSIL HSJL

,~ ____ c_1N_1
___ ~I J CIN 2 I LI ____ c_,N_3
___ ~

I Normal squamous epithelium I Dysplasia

III. RISKFACTORS
• Compromised immune system (genetic, iatrogenic, infectious)
• Increased risk for acquiring HPV infection:
Early age of first sexual intercourse (<14 years old)
0 Early age at first full term pregnancy ( <17 years old)
Lifetime number of sexual partners (<!2partners)
History of and/or co-infection with other sexually transmitted infections (e.g., herpes
simplex, chlamydia and gonorrhea)
Long-term use of oral contraceptive pill (OCP) (>5 years)
History ofvulvar or vaginal dysplasia
Smoking (Squamous Cell CA,not Adena CA)
0 Uncircumcised male partner

486
PREVENTION OF INTRAEPITHELIAL NEOPLASIA
• Cervical cancer is a preventable disease, with excellent tools for prevention (i.e.,
vaccination) and screening (i.e., Pap and human papillomavirus testing)

I. PRIMARY PREVENTION
A. Education and Counseling
• Sexual abstinence
• Lifetime monogamous sexual relationship
• Delay in onset of sexual intercourse
• Use of barrier contraceptive methods (e.g., condom)

B. HPV Vaccination
• Bivalent vaccine or Cervarix® (targets HPV types 16,18)
• Quadrivalent vaccine or Gardasil® (targets HPV types 6,11,16,18)
• Nonavalent vaccine or Gardasil-9® (targets HPVtypes 6, 11, 16, 18, 31, 33, 45, 52, and 58)

HPV Vaccination Schedule:

BIVALENT QUADRIVALENT
I VACCINE
I VACCINE I NONAVALENT VACCINE

HPV6/11/16/18/
HPVTypes HPV 16/18 HPV 6/11/16/18
31/33/45/52/58

Sex&Age
Indication Female I :e15y/o
Female
Male
I 14-45 y/o
I 14-26 y/o
Female
Male
I
I
"15 y/o

Dosage 0, 1, 6 months 0, 2, 6 months 0, 2, 6 months

Sex&Age
Female 19-14 y/o
Female I 9-14 y/o Female I 9-14y/o
Indication Male I Male I
Dosage 0, 5-13 months 0, 6 or 0,12 months 0, 5-13 months

II. SECONDARY PREVENTION: SCREENING

A. Modes of Screening/Testing for Cervical Cancer or HPV

MODALITY I REMARKS
• Most widely used screening test
• Has low sensitivity, but widespread testing has reduced
Cervical cytology
incidence of cervical cancer by 50- 70%
testing
• Performed by placing a speculum into the vagina and scraping
(Pap smear)
cervical cells using a spatula and endocervical brush
• Cells are sampled from the transformation zone
• May be more sensitive than Pap smear, but co-testing with HPV is
PrimaryHPV also recommended
testing • Preferred screening method in countries where Pap smear is not
feasible and HPV testing is available
Gynecology17thEd; 2017
LoboRA.Comprehensive

I
487
B. Guidelines for Cervical Cancer Screening

WHO 2021 Guidelines for Screening and Treatment of Cervical Pre-Cancer Lesions for
Cervical Cancer Prevention
<30years
old, general • No screening
population
• HPV DNA detection in a screen-and-treat approach starting at the age of
30 with regular screening every 5 to 10 years
• HPV DNA detection in a screen, triage, and treat approach starting at the
30-50years
age of 30 yeas with regular screening every 5 to 10 years
old
• Where HPV DNA testing is not yet operational, WHO suggests a regular
screening interval every 3 years when using vaginal inspection with
acetic acid (VIA} or cytology as the primary screening test
• WHO suggest screening is stopped after two consecutive negative
After 50
screening results consistent with the recommended regular screening
years old
intervals among both the general population and women living with HIV
• HPV DNA detection in a screen, triage, and treat approach starting at the
age of 25 years with regular screening every 3 to 5 years
Women
• Where HPV DNA testing is not yet operational, WHO suggests a regular
with HIV
screening interval every 3 years when using VIA or cytology as the
primary screening test

WHO2021 Guidelinefor Screeningand Treatmentof CervicalPre-cancerLesionsfor CervicalCancer Prevention

ACS 2020 Cervical Cancer Screening Recommendation

<25 years old • No screening
• Primary HPV test alone every 5 years (preferred)
• Use an FDA approved HPV test for primary screening
.: 25 to 65 years old
• Acceptable options: co-testing (HPV testing in combination
with cytology) every 5 years or cytology alone every 3 years
> 65 years old with
• Discontinue cervical cancer screening with any modality if
• no history of CIN grade
with adequate negative prior screening*
2 or a more severe
• Individuals aged >65 years without documentation of prior
diagnosis within the past
screening should continue until criteria for cessation are met
25 years, and
• documented adequate
negative prior screening*
in the 10 year period
before age 65 years old
• Follow age-specific screening recommendations (same as
After HPVvaccination
unvaccinated individuals)
• Individuals without a cervix and without a history of CIN 2
After hysterectomy or a more severe diagnosis in the past 25 years or cervical
cancer ever should not be screened
'2 consecutivenegativeprimaryHPVtests, or
2 consecutivenegativeco-tests,or
3 consecutivenegativecytologytests withinthe past 10 years, withthe most recenttest occurringwithingthe past
3-5years,dependingon the recommendedintervalforthe test used

Fonthamet al. CervicalCancer Screeningfor Individualsat AverageRisk:2020 Guideline

Updatefromthe AmericanCancer Society.

488
CERVICAL CYTOLOGY REPORTING: THE 2014 BETHESDA SYSTEM
• First part states whether the sample is satisfactory or unsatisfactory
• Next part indicates whether cellular material is normal
• Abnormalities are divided into squamous and glandular
• Other comments may also include evidence of infection (e.g., yeast, bacterial vaginosis)

I. PAP SMEAR SAMPLE REPORT THE BETHESDA SYSTEM 2014

Page 1 of2
SPECIMEN TYPE:
Indicate convelllional smear (Pap smear) vs. liquid-based preparation vs. other

SPECIMEN ADEQUACY
- Satisfactory for evaluation (describe presence or absence of endocervica/lrransformation
zone component and any other quality indicators, e.g., partially obscuring blood,
inflammation, etc.)
D Unsatisfactory for evaluation ... (specif.i•reason)
J Specimen rejected/not processed (speciji• reason)
J Specimen processed and examined, but unsatisfactory for evaluation of epithelial
abnormality because of (specify reason)

GENERAL CATEGORIZATION (optional)

_ Negative for lntraepithelial Lesion or Malignancy
Other:See interpretation/result(e.g., endometrial cells in a woman ?.45 years old)
=::;
D Epithelial Cell Abnormality: See interpretation/result (specify 'squamous' or 'glandular'
as appropriate)

INTERPRETATION/RESULT
NEGATIVE FOR INTRAEPITHELIAL LESION OR MALIGNANCY
(When there is no cellular evidence of neoplasia, state this i11the General Categorizatio11 above
and/or in the lnrerpretation!Result section of the report - whether or not there are organisms or
other 11011-neoplasticfi11di11gs)

Non-neoplastic Findings (optional to report)

= Non-neoplasticcellular variations
C Squamous metaplasia
C Keratotic changes
D Tubal metaplasia
0 Atrophy
L Pregnancy-associated changes
D Reactive cellular changes associated with:
C Inflammation (includes typical repair)
C Lymphocytic (follicular) cervicitis
l Radiation
C Intrauterinecontraceptive device
!J Glandular cells status post-hysterectomy

Orga11isms
□ Trichomonas vagina/is
7 Fungal organisms morphologically consistent with Ca11didaspp.
'.J Shift in flora suggestive of bacterial vagjnosis
J Bacteria morphologically consistent with Actinomyces spp.
□ Cellular changes consistent with herpes simplex virus

■
D Cellular changes consistent with cytomegalovirus

OTHER
J Endometrial cells (in a woman ;,45 years old)
(Specify if '11egativefor squamous i11traepithelial lesion)

489
 Page 2 of2
EPITHELIAL CEU ABNORMAL/TIES

Squamous Cell
□ Atypical squamous cells
0 Of undetermined significance (ASC-US)
D Cannot exclude HSIL (ASC-H)
□ Low-grade squamous intraepithelial lesion (LSIL)
(encompassing HPV!mild dysplasia/C!N I)
□ High-grade squamous intraepithelial lesion (HSIL)
(encompassing moderare and severe dysp/asia, CIS; CIN 2 and CIN 3)
□ With features suspicious for invasion (if invasion is suspected)
□ Squamous cell carcinoma

Glandular Cell
□ Atypical glandular cells
0 Endocervical cells (NOS or specify in commenls)
□ Endometrial cells (NOS or specify in commenrs)
□ Glandular cells (NOS or specify in comments)
□ Atypical glandular cells
□ Endocervical cells, favor neoplastic
□ Glandular cells, favor neoplastic
□ Endocervical adenocarcinoma in situ
0 Adenocarcinoma
0 Endocervical
0 Endometrial
0 Extrauterine
0 Not otherwise specified (NOS)

OTHER MALIGNANT NEOPLASMS: (specify)

ADJUNCTIVE TESTING
Provide a brief descriprion of rhe res/ method(s) and report rhe result so thar ii is easily
understood by the clinician.

COMPUTER-ASSISTED INTERPRETATION OF CERVICAL CYTOLOGY

If case examined by an automated device, specify device and result.

EDUCATIONAL NOTES AND COMMENTS APPENDED TO CYTOLOGY REPORTS

(optional)
Suggestions should be concise and consisrenl with clinical follow-up guidelines published by
professional organizations (references to relevanr publicarions may be included)

490
II. DESCRIPTIONAND MANAGEMENTOF SPECIFICABNORMALITIES

PAP SMEAR
OR CYTOLOGY
FINDINGS
I REMARKS
I MANAGEMENT*

• Repeat age-based screening after 2 to 4

• Specimen processed months, if any of the following:
and examined, Not tested for HPVor unknown HPVresult
0

but unsatisfactory HPV negative (>25 y/o)

0
Unsatisfactory
for evaluation HPVpositive (>25 y/o), unknown genotype
0

of epithelial • Refer for Colposcopy**, if:

abnormality. HPVpositive (>25 y/o), unknown genotype
0

HPV 16 or 18 positive
0

Squamous Cell Abnormalities

• Repeat age-based screening after 2 to 4
• Atypical squamous months, if any of the following:
cells of undetermined Not tested for HPV or unknown HPV
0

significance (ASC-US): result

few cells associated HPV negative (>25 y /o)
0

with squamous HPV positive (>25 y/o), unknown

0

Atypical intraepithelial lesions genotype

squamous but not consistent • Refer for Colposcopy**, if:
cells of with a more precise HPV positive (>25 y/o), unknown
0

undetermined diagnosis (most genotype

significance common squamous HPV 16 or 18 positive
0

(ASC-US) abnormality) If pregnant, defer until 6 weeks

0

postpartum
• Atypical squamous
cells, cannot exclude • Refer for colposcopy** regardless of HPV
a higher-grade lesion status
(ASC-H)
• Indicates more
High-grade • Immediate Loop Electrosurgical Excision
severe dysplasia or
squamous Procedure (LEEP), except if patient is
CIN 2/3
intraepithelial pregnant or age 21-24, OR
lesion (HSIL) • 20% may progress
• Refer for colposcopy**
to cervical cancer
Glandular,Cell Abnormalities
• Plus any subcategories: atypical
endocervical cells or atypical glandular cells
(except atypical endometrial cells):
Refer for colposcopy** and endometrial
0

• May be classified
Atypical sampling (if>35 y/o or <35 y/o and at
by the site of origin
glandular cells risk for endometrial neoplasia: obesity,
(e.g., endometrium,
(AGC) abnormal uterine bleeding, or conditions
endocervix, ovary)
suggesting chronic anovulation.)
• Plus atypical endometrial cells:
Endometrial and endocervical biopsy
0

Refer for colposcopy**

0

• Maydownload ASCCPscreening appinAppleAppStoreor GooglePlayStore

■
"Colposcopyis oftenthefirststepin evaluation
of womenwithabnormalcytology.Colposcope (lightedmagnified
instrument)
is usedto examinethecervix,placedjust outsidethevaginaaftera speculumis inserted.Thisis
performed
by a certifiedOB-GYNColposcopist.
Source:AmericanSocietyof Colposcopy
andCervicalPathology
(ASCCP);2012;2019
LoboRA.ComprehensiveGynecology
17thEd;2017

491
III. LOW-GRADESQUAMOUSINTRAEPITHELIAL LESION(LSIL}CYTOLOGY
• Management varies based on previous and current HPV status, previous cytology result,
and previous biopsy result

HPVRESULT
(Current)
~ RECOMMENDATION
Unknown -
Negative
Follow-up after 1
Negative ASCUS
year
Negative Negative LSIL
Positive NILM
Follow-up after 1
- - CIN 2 or 3 year, if previously
treated
Unknown Refer for colposcopy
Negative - - Follow-up after 1
Negative ASCUS - year
Positive Negative LSIL
Refer for colposcopy
Positive NILM
Refer for colposcopy,
- - CIN 2 or 3
if previously treated
AdaptedfromASCCP2019

IV.HIGH-GRADESQUAMOUSINTRAEPITHELIAL LESION(HSIL) CYTOLOGY

• HSIL has the highest risk for cervical intraepithelial neoplasia and cervical cancer
• Immediate loop electrocautery excision procedure (LEEP) should be done
• Ablation should not be done because ablative procedures do not provide a specimen for
histologic evaluation
• Colposcopy with endocervical assessment may also be done
• In pregnant patient, colposcopy without endocervical assessment is done

492
CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN)
• CIN is the precancerous lesion of the squamous epithelium of the cervix
• It is a histologic (versus cytologic) diagnosis, based on tissue examination of a cervical
biopsy specimen
• Graded 1, 2, or 3 (depending on how much of the epithelial layer contains atypical cells)

Molecular factors: oncoproteins

E6 binds to p53 leading to apoptosis
. E7 releases E2Ffrom pRb leading to cycle progression
Riskfactors
STD,HIV,smoking, immunosuppressed state

HPVinfection lOOOx Annual HSILto

more common carcinoma
Persistence
than LSIL progression: 1.4%

Infection ("\ Progression

INormal cell I, I LSIL I I HSIL.
I
Invasion
iiii%Hi&i
Clearance Regression

HPVcleared 93% Latency and incubation to

by 3 years cancer within 15 years

• CIN 1 (mild dysplasia): usually regresses spontaneously within weeks to months

• CIN 2 (moderate dysplasia): cellular atypia involves 2/3 of the thickness of epithelium,
which may still be reversible
• CIN 3 (severe dysplasia or carcinoma in situ): cellular atypia involves >2/3 of the
epithelium, which is a precursor to invasive cancer

Approach to Cervical lntraepithe/ial Neoplasia

LESION I Women 25 years old and older I Women 21-24 years old
• Follow up without treatment
CIN 1
• Do co-testing with cervical • Follow up without treatment
Preceded by:
cytology and HPV testing in 12 • Repeat cytology after 1 year
ASCUS, LSIL
months
• If adequate colposcopy with ECC
negative: co-testing at 12 & 24
CIN 1 • If with adequate colposcopy and
months
Preceded ECCnegative: Colposcopy and
• Diagnostic Excisional Procedure
byASC-H or cytology at 6 month intervals
(LEEP/Cone Biopsy)
HSIL until 24 months
• Review of cytologic, histologic, and
colposcopic findings
With adequate colposcopy (entire squamocolumnar junction is visible
circumferentially around the external cervical os.
• Ablation or excision, OR
• Observation for up to 12 months
• Ablation or Excision
using both colposcopy & cytology
CIN 2 or 3 at 6 month intervals

■
With inadequate colposcopy, recurrent CIN2,3 or ECCis CIN2, 3
• CIN2: Observation for up to 12
months using both colposcopy
• Diagnostic excisional procedure
and cytology at 6 month intervals
• CIN3: Ablation or Excision
Source:AmericanSocietyforColposcopyand CervicalPathology;2013
493
CERVICAL ADENOCARCINOMA IN SITU
• Adenocarcinoma in situ (A!S) is a premalignant precursor to cervical adenocarcinoma
• The glandular architecture of the endocervical glands are preserved in A!S, but the glands
are lined by atypical columnar epithelial cells

Approach to Cervical Adenocarcinoma in Situ

• Management is difficult because of the multi focal nature of A!S, which means that negative
margins on an excisional specimen is not an assurance that complete excision has been achieved
• An excisional procedure must be done and subsequent steps as follows:
EXCISIONAL BIOPSY WITH POSITIVE I EXCISIONAL BIOPSY WITH NEGATIVE
MARGINS OR POSITIVE ECC MARGINS
• Hysterectomy (preferred)
• Re-excision until with negative margins 0 HPV based testing annually x 3 years, then every
is preferred ( even if with plans to 3 years for at least 25 years
proceed with hysterectomy) • If desirous of pregnancy:
0 If with persistent positive margins, 0 Re-evaluation ( co-testing with endocervical
or re-excision not possible, simple sampling) every 6 months x 2 years, then annually
total hysterectomy or modified radical x 2 years is acceptable; if with all negative
hysterectomy is acceptable results may do every 3 years until hysterectomy
0 Hysterectomy should be done followingchildbearing
ForAIS,hysterectomyis the treatmentof choice.Conservativemanagementis onlyacceptable if patientis desirous
of pregnancybut hysterectomyshould be done after childbearing.
Source:AmericanSocietyfor Colposcopyand CervicalPathology;2013

MANAGEMENT FOR CERVICAL DYSPLASIA

• CIN 1 should be observed, rather than treated, because it usually regresses spontaneously
• CIN 2 or 3: treated with ablation (e.g., cryotherapy) or excision (e.g., loop electrosurgical
excision [LEEP], cold knife conization [CKC])
• LEEP is the most common method for treatment ofCIN 2 or 3

I. ABLATIVEAND EXCISIONAL
PROCEDURES

Criteria/Indication '[or Procedure

• No suspicion of glandular involvement or
invasive cancer
• Satisfactory colposcopy with visualization
of entire cervical squamocolumnar junction
• Biopsy confirming presence ofCIN;
abnormal cytology alone is not sufficient
• Lesion does not involve the endocervical
canal and is negative on endocervical
curettage
Procedures
• Cryotherapy
• CO, ablation
• Unable to rule out invasive disease
• AdenoCAin situ or other glandular abnormalities
• Unsatisfactory colposcopy in which the
transformation zone is not fully visualized
• Lack of correlation between cytology and
colposcopy / biopsies
• Lesion extending into the endocervical canal
• Endocervical curettage showing CIN or a
glandular abnormality
• Recurrence after an ablative or previous
excisional procedure
• Loop Electrosurgical Excision Procedure (LEEP)
• Cold-knife Conization (CKC)

II. FOLLOW-UP
• Rate of recurrent or persistent disease following excisional or ablative treatment for C!N
2/3 is 5-17%, with no significant differences in outcomes between the different treatments
• Co-testing with cervical cytology and HPVat 12 and 24 months:
If both co-tests are negative, the woman can return to routine screening
0

0 If any test is abnormal, colposcopy with endocervical sampling is recommended

494
VULVAR ATYPIA
ETIOPAlHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT

Liche11.Sclerosus
• 5%-15% ofpostmenopausal • Pruritus • Biopsy • High potency
women • Diffuse whitish topical steroids:
• Cumulative incidence of skin 0.05% Clobetasol
squamous cell carcinoma of the • Skin appears thin proprianote
vulva~ 6.7% • May have ointment
• Latency period between scarring, • Topical calcineurin
diagnosis and subsequent vulvar contracture, inhibitors (TCls)
cancer~ 3 years fissuring and/or • Testosterone cream
• Standard incidence ratio of excoriation • Progesterone cream
developing vulvar cancer= 33.6
• Epithelium markedly becomes
thinned with loss or blunting
of the rete ridges; thickening or
hyperkeratosis of surface layers;
inflammation present
Squamous Cell Hyperplasia (formerly called hyperpla~tic dystrophy without atypici)
• Hyperplasic dystrophy • Chronic pruritus • Biopsy • Medium potency
• Elongation & widening of rete • Whitish lesions topical steroids:
ridges, which may be confluent • Thickened skin Triamcinolone
• Focal or acetonide or
multifocal rather Fluocinolone
than diffuse acetonide

. Pf!.get'sDisease* (see n_oteson next page) -

• Rare intraepithelial disorder • Itching, irritation • Biopsy • Surgery-
in vulva and burning Wide local excision
• Histologically resembles Paget • Reddish with removal of
disease of breast eczema to id underlying dermis
• Associated with underlying appearance of at least 4-6 mm
invasive adenocarcinoma of vulva, • Erythematous depth and frozen
vagina & anus, as well as distant plaque with section of surgical
sites, including bladder, cervix, typical white margins
colon, stomach and breast scaling known
• Paget cell - large pale cells as "cake-icing
occurring in nests and infiltrate scaling"
upward through the epithelium
,s~uamouslntraJP,i!/l_eJ!gl,Lesiqn
{SIL}/ Vul'(_pr,!ntraepithelia_,l
ie;;on {VIN)**(seenotes_onnextpag_;J
• HPV-related • Variable clinical • Biopsy • Surgery -
• Atypical changes in the appearance: Wide Local Excision
epithelium marked by a loss of white, red or
the maturation process as well pigmented areas
as increase in the mitotic activity • Lesions tend to
and nuclear/cytoplasmic ratio be discrete and
• VIN 1: Mild dysplasia (atypia) - multifocal
lower 3rd of the epithelium
• VIN 2: Moderate dysplasia
(atypia) - half to 2/3 of the

■
epithelium
• VIN 3: Severe dysplasia
(atypia) - more than 2/3 of the
epithelium; Carcinoma-in-situ -
full thickness of the epithelium
Sources:vanderLindenet al. PagetDiseaseof theVulva,CntRevOneHem,2016
Gershenson et al. Comprehensive
Gynecology,
8thEd,2022.

495
*Wilkinson Classification of Vu/var Puget's Disease (VPD)

Type la Cutaneous vu Ivar non-invasive Paget's disease

Cutaneous vulvar invasive disease; dermal invasion of

PrimaryVPD Type lb
Paget cells
(cutaneous)
Cutaneous vulvar disease as a manifestation of an
Type le
underlying vulvar adenocarcinoma

Secondary VPD Type2 VPD originates from rectal or anal adenocarcinoma

(non-cutaneous) Type3 VPD originates from urogenital neoplasia
Source:vanderLindenet al. PagetDiseaseof theVulva,GritRevOneHem,2016

**Classfications of Vu/var lntraepithelial Lesions

2004 Terminology I LAST (2013) I ISSVD (2015) I WHO (2020)
Flat condyloma or HPV-
LSIL (VIN 1) LSIL (VIN 1) LSIL (VIN 1)
associated vulvar lesions
Usual type (subdivided):
VIN, warty type
VIN, basaloid type HSIL (VIN 2,3) HSIL (VIN 2,3) HSIL (VIN 2,3)
VIN, mixed (warty or
basaloid) type
Differentiated-type VIN ---
Differentiated- Differentiated-
(DVIN) type VIN (DVIN) type VIN (VIN)
LAST- LowerAnogenital Squamous Terminology; WHO- WorldHealthOrganization;
ISSVD- International
Societyfor theVulvovaginal
Disease
LSIL- Low-grade squamous lesion;HSIL- High-grade
intraepithelial squamous
intraepithelial
lesion
Source:CPGfor theObstetrician-Gynecologist,
3rdEd,SGOP,2019
FemaleGenitalTractTumors,fromtheWHOClassificationof TumorsSeries,5th Ed,2020.

496
 SECTION TWO
CERVICAL CARCINOMA
CERVICAL CARCINOMA
• Cervical carcinoma is the third most frequent malignancy of the lower female genital tract
(after endometrial and ovarian cancer)
• It is the 2nd most frequent cause of death (after ovarian cancer)

I. RISK FACTORS
• Persistent high risk HPV type (necessary cause of cervical cancer)
• Parity of 7 or more
• 0CP use >S years with HPV
• Current smokers & younger age at smoking
• Co-infected with Chlamydia or HSV-2
• HIV
• Early age at sex <14 years old
• Lifetime number of sexual partners 2:2
• First pregnancy <17 years old
• No cervical cancer screening
• Low socio-economic status
• Poor access to healthcare services, poor nutrition, etc.

II. WHO HISTOLOGICAL

CLASSIFICATION
OF TUMORSOF THE UTERINECERVIX
Majority of cervical malignancies are carcinomas
• Most are squamous cell carcinomas, but the incidence of adenocarcinomas has increased
in most developing countries
I HISTOLOGIC FEATURES I CATEGORY
• Large cell (keratinizing or non-
keratinizing)
• Arising from ectocervix • Basaloid
Squamous Cell • Most common (85-90%) • Verrucous
Carcinoma • Most are of the large cell, • Warty
non-keratinizing type • Papillary
• Lymphoepithelioma-like
• Squamotransitional
• Mucinous
• Endocervical
• Intestinal
• Signet-ring cell
• Arising from • Minimal deviation (Adenoma
Adenocarcinoma endocervical columnar malignum)
epithelium (10-15%) • Villoglandular
• Endometrioid
• Clear cell
• Serous
• Mesonephric
• Adenosquamous carcinoma
• Glassy cell carcinoma variant
• Adenoid cystic carcinoma
• Adenoid basal carcinoma

■
• Neuroendocrine tumors
Other (mixed)
epithelial tumors --- • Carcinoid
0 Atypical carcinoid

• Small cell carcinoma

0 Large cell neuroendocrine

carcinoma
• Undifferentiated carcinoma
497
MANIFESTATIONS AND STAGING
I. SIGNSAND SYMPTOMS
• Irregular spotting or light bleeding between periods in women of
reproductive age
Symptoms in
• Postmenopausal spotting or bleeding
the early stages
• Bleeding after sexual intercourse
• Increased vaginal discharge (sometimes foul-smelling)
• Persistent back, leg and/or pelvic pain
• Weight loss, fatigue, loss of appetite
Symptoms in • Foul-smelling vaginal discharge and discomfort
the late stages • Swelling of a leg or both lower extremities
• Other severe symptoms may arise at advanced stages depending on
which organs cancer has spread
• Visible and/or palpable cervical lesion/mass
Exophytic growth or cauliflower-like
0
Signs
Endophytic growth or barrel-shaped
0

Infiltrative growth with central excavation

0

II. HISTORYAND PATTERNOF SPREAD

• Cervical carcinoma is initially a locally infiltrating cancer that spreads from the cervix to
the vagina and paracervical/parametrial areas
• Spread may be:
0 Direct spread to adjacent tissues like uterus, vagina, parametria, bladder, rectum
Lymphatic spread
Hematogenous spread

498
II. THE UNION FOR INTERNATIONALCANCERCONTROL (UJCC) TNM AND FJGO 2018
STAGINGCLASSIFICATIONOF CERVICALCANCER

T I
FIGO
CATEGORY STAGE
I DEFINITION

TX • Primary tumor cannot be assessed

TO • No evidence of primary tumor
• The carcinoma is strictly confined to the cervix (extension to the
Tl I
corpus should be disregarded)
• Invasive carcinoma that can be diagnosed only by microscopy
Tla IA
with maximum depth of invasion ,; 5 mm'
Tlal IAl • Measured stromal invasion of,; 3.0 mm in depth
T1a2 IA2 • Measured stromal invasion of> 3.0 mm and,; 5.0 mm in depth
• Invasive carcinoma with measured deepest stromal invasion
Tlb 1B > 5.0 mm (greater than stage IA); lesion limited to the cervix
uteri with size measured by maximum tumor diameterh
• Invasive carcinoma> 5.0 mm depth of stromal invasion and,; 2.0
Tlbl IBl
cm in greatest dimension
IB2 • Invasive carcinoma> 2.0 cm and,; 4.0 cm in greatest dimension
T1b2
IB3 • Invasive carcinoma> 4.0 cm in greatest dimension
• The cervical carcinoma invades beyond the uterus, but has not
T2 II
extended onto the lower third of the vagina or to the pelvic wall
• Involvement limited to the upper two-thirds of the vagina
T2a HA
without parametrial invasion
T2al IIAl • Invasive carcinoma,; 4.0 cm in greatest dimension
T2a2 IIA2 • Invasive carcinoma > 4.0 cm in greatest dimension
T2b 11B • With parametrial invasion but not up to the pelvic wall
• The carcinoma involves the lower third of the vagina and/or
extends to the pelvic wall and/or causes hydronephrosis or non-
T3 III
functioning kidney and/or involves pelvic and/or para-aortic
lymph nodes
• Carcinoma involves lower third of the vagina with no extension
T3a IIIA
to the pelvic wall
• Extension to the pelvic wall and/or hydronephrosis or non-
IIIB
functioning kidney (unless known to be due to another cause)
• Involvement of pelvic and/or para-aortic lymph nodes
(including micrometastases)", irrespective of tumor size and
T3b me extent
(with rand p notations)•
IIICl • Pelvic lymph node metastasis only
IIIC2 • Paraaortic lymph node metastasis

■
t1/ • The carcinoma has extended beyond the true pelvis or has involved
IV (biopsy proven) the mucosa of the bladder or rectum. A bullous
edema, as such, does not permit a case to be allotted to Stage IV
T4
IVA • Spread of growth to adjacent organs
IVB • Spread to distant organs

499
Notes on Cervical Cancer Staging
'Imagingandpathology canbe used,whenavailable,to supplement
clinicalfindingswithrespectto tumorsizeand
extent,in all stages.Pathological
findingssupercede
imagingandclinicalfindings

of vascular/lymphatic
'The involvement spacesshouldnotchangethestaging.Thelateralextentof the lesionis no
longerconsidered

'The pelvicsidewallis definedas the muscle,fascia,neurovascular

structuresandskeletalportionsof the bony
pelvis

'Isolatedtumorcellsdo notchangethestagebuttheirpresenceshouldbe recorded

'Addingnotationof r (radiologic
or sonographicimaging)andp (pathology)
to indicatethefindingsthatareusedto
allocatethecaseto stageIIIC.Exampleif imagingindicatespelviclymphnodemetastasis, stageallocation
would
be stageIIIC1rand if confirmedby pathologic
findings,casewouldbe stageIIICp.Typeof imagingmodalityand
pathologictechniqueusedshouldalwaysbe documented
Source:8theditionof the Unionfor International
CancerControl(UICC)TNMclassification of malignant
tumours;2016
RevisedFIGOstagingfor carcinomaof thecervixuteri.IntJ GynaecolObstet2019

MANAGEMENT
STAGE I MANAGEMENT
• Desirous of pregnancy with no Lymphovascular Space Invasion (LVSI)
0 (-) margins: observe
0 ( +) margins: repeat cone biopsy or do trachelectomy

• Desirous of pregnancy with LVSI

0 (-) margins: bilateral pelvic lymph node dissection (BLND)
0 ( +) margins: repeat cone biopsy or do trachelectomy + BLND ±
!Ala
paraaortic lymph node sampling (PALS)
• Not desirous of pregnancy
0 Extrafascial Hysterectomy (EH), Bilateral Salpingectomy (BS) ±

Bilateral Oophorectomy (BO)

0 If ( +) LVSI: Radical Hysterectomy (RH) + Bilateral Salpingo-

oophorectomy (BSD) + BLND + PALS

• Desirous of pregnancy
0 Radical vaginal or abdominal trachelectomy + BLND + PALS

IA2' • Not desirous of pregnancy

0 Radical hysterectomy with bilateral salpingectomy (RHBS) + BLND

+ PALS± BO

• RHBS + BLND +PALS± BO or

IB1, IB2, IIAl • Concurrent chemotherapyb and Pelvic External Beam Radiotherapy
(EBRT) + Brachytherapy (Chemoradiation)'
• Chemoradiation
• If (+) paraaortic lymphadenopathy (size> 1.0 cm) by MRI, CTscanor PET-CT
IB3, IIAZ-IVA scanconfirmed by fine needleaspiration biopsy (FNAE) or extraperitoneal
or laparoscopic lymphadenectomy: Concurrent chemotherapyb and
,, Extended Field Radiotherapy (EFRT) + Brachytherapy

• Cisplatin-based chemotherapy+ individualized RT for control of

IVB
pelvic disease and other symptoms
•StagesIA1 andIA2arediagnosed by diagnostic
excisionalprocedures.
'Standardchemotherapy drugto usefor concurrent
treatmentwithradiotherapy
(chemoradiation,
CCRT):Cisplatin
40 mglm'givenweeklyduringpelvicEBRTor EFRT
'Chemoradiation
is thecurrentstandardof careandmainstayof treatment.

NOTE:Forpatientswhowillundergoa surgicalintervention,
postoperative will be dependent
chemoradiation onthe
presenceof surgicopathologic
factors. e

500
ENDOMETRIAL HYPERPLASIA
I. ETIOPATHOGENESIS
• Endometrial hyperplasia results from an excess of estrogen or an excess of estrogen
relative to progestin (such as occurs with anovulation)
• Two important separate categories:
Atypical hyperplasia
0 Hyperplasia without atypia

I Benign endometrium I
Unopposedestrogen TP53
(irregular ovulation/ I mutations
anovufotion, obesity)

Non-typical hyperplasia Atrophic endometrium

PTEN, MLHl, MSH6, ras mutations TP53 mutation
Clonal expansion Her2/neu amplification

Complex atypical hyperplasia Glandular dysplasia

KRAS,beta cateninmutations TP53 mutation

Microsatellite instabilities Her2/neuamplification

Endometrioid carcinoma Gl Serous intraepithelialcarcinoma

TP53, Her2/neu mutations TP53, P/3K, PPP2RlA,

Parocrinestromol effect FBXW7mutations
Her2/neu, Pl6, GLUTl,
HMGAZ amplification

Endometrioid carcinoma G3, Uterine serous

Mixed endometrioid/ ----• carcinoma
serous/clear cell type TP53 (USC)
mutation?

II. PATHOLOGY
A. Pathologic Features
PATHOLOGY I CHARACTERISTIC
• Irregularity in the shape of glands with cystic alterations
• Abundant stroma between glands
• Glands cystically dilated with occasional outpouchings and
Simple hyperplasia
focal crowding
• Lined by pseudostratified tall columnar epithelium
• Glands separated by abundant cellular stroma

• Highly crowded glands with little stroma

• Complex glandular outlines with papillary intraluminal
Complex hyperplasia
folding
• Pseudostratified tall columnar epithelium lined glands

• Loss of polarity

■
• Increased nucleus:cytoplasm (N:C) ratio
Atypia* • Irregular size and shape
• Prominent nucleoli
• Thick nuclear membrane
'Cytologicatypia in endometrialhyperplasiais the most importantfactor in determiningmalignantpotential

501
 B. Endometrial Intraepithelial Neoplasia (EIN) Criteria
EIN CRITERIA I COMMENTS

Architecture • Area of glands> stroma (volume percentage stroma < 55%)

Cytology • Cytology differs between architecturally crowded focus and background
Size> 1 mm • Maximum linear dimension exceed 1 mm
• Benign conditions with overlapping criteria (ie, basalis, secretory,
Exclude mimics
polyps, repair)
Exclude cancer • Carcinoma if maze-like glands, solid areas or appreciable cribriforming

III. WHO 2014 CLASSIFICATION OF ENDOMETRIAL HYPERPLASIAS

NEW TERM SYNONYMS

GENETIC ICOEXISTENT
INVASIVE
ENDOMETRIAL
IPROGRESSION
TO INVASIVE
CHANGES
I I CARCINOMA CARCINOMA

• Benign
endometrial
hyperplasia
• Simple
non-atypical
endometrial
• Low level
hyperplasia
of somatic
• Complex
mutations
non-atypical • Weakly pre-
in scattered
Hyperplasia endometrial malignant
glands with
without hyperplasia • <1% • Relative risk
atypia
morphology
• Simple (RR):
on HE
endometrial 1.01-1.03
staining
hyperplasia
showing no
without
changes
atypia
• Complex
endometrial
hyperplasia
without
atypia
• Many of
the genetic
changes
• Complex typical for
atypical endometrial
endometrial cancer • Complex
Atypical hyperplasia (endometrioid atypical
hyperplasia / • Simple type) are hyperplasia
Endometrial atypical present, • 25-33% has the
Intraepithelial endometrial including • 59% greatest
Neoplasia hyperplasia microsatellite malignant
(EIN) • Endometrial instability; potential
intraepithelial PAXZ • RR: 14-15
neoplasia inactivation;
(ElN) mutation of
PTEN,KRAS
and CTN NB1
(~-catenin)

502
III. DIAGNOSIS
DIAGNOSTIC
Endometrial biopsy
Pelvic Ultrasound with
Dopplers using the IETA
I REMARKS
• Types include:
0 Hysteroscopic-targeted biopsy
0 Ultrasound-guided biopsy
0 Office biopsy
0 Endometrial curettage
• Primary tool for evaluation of abnormal uterine bleeding

IV. MANAGEMENT
I POSTMENOPAUSAL
HISTOLOGIC
TYPE I PREMENOPAUSAL
WOMEN
• Levonorgestrel-releasing Intrauterine System
WOMEN

[LNG-IUS)- releases progesterone

15-20 ug/day x 3-6 months OR
• Megestrol acetate 40-160 mg OD x 3-6
months OR
• Medroxyprogesterone acetate [MPA)
10-20 mg OD x 3-6 months OR 10 mg OD x
• Extrafascial
12-14 days each month x 3-6 months OR
Hyperplasia hysterectomy with
• Depot-MPA 150 mg IM every 3 months
without bilateral salpingo-
atypia • Do UTS & endometrial sampling to document
oophorectomy
regression to normal endometrium every
[EHBSO)
3 months. Maintenance treatment after
regression to normal endometrium is 6-12
months. If regression to normal endometrium
does not occur after 3-6 months, the
progestin dose may be increased. If atypia is
noted or endometrial cancer develops, the
patient should be managed appropriately.
• If desirous of pregnancy
0 Megestrol acetate 80 mg BID or 160 mg OD
x 3-6 months; may increase to 160 mg BID
if no regression after 3 months
0 MPA10-20 mg OD continuously x 3-6 months
0 LNG-JUS-releases 15-20 ug/day x 3-6 months
0 Do UTS & endometrial sampling
to document regression to normal
Hyperplasia
endometrium every 3-6 months. If • EHBSO
withatypia
regression to normal endometrium does
not occur after 3-6 months, the progestin
dose may be increased. If atypia is
present despite the increase in dosage or
endometrial cancer develops, the patient
should be managed appropriately.
• Not desirous of pregnancy:
EHBS+ /- Bilateral oophorectomy
ForProgestin-resistantcases, optionsmayincludethefollowing:
1. Danazol400 mgdailyx 3-6months
2. GnRHanalogues+Progestincombination
• Norethisterone

or Leuprolin
acetate500mgweeklyx 3-6monthsPLUS
• Goserelin3.6 mgor Leuprolin3.75mgor Triptorelin
11.25mgor Triptorelin
3.75mgevery28 daysx 6 monthsORGoserelin10.8mg
11.25mgdepotevery3 monthsx 6 monthsORTriptorelin
22.5mgsingle
I
dose

503
ENDOMETRIAL CANCER
• Endometrial carcinoma is the most common malignancy of the female genital tract
• Adenocarcinoma of the endometrium affects women primarily in the perimenopausal
and postmenopausal years (most frequent in the ages of SO to 65 years)

I. ETIOPATHOGENESIS
INCREASES THE RISK I DIMINISHES THE RISK
• Unopposed estrogen stimulation of the • Monthly ovulation and menstruation
endometrium • Progestin therapy
• Unopposed menopausal estrogen • Combination oral contraceptive pills
replacement therapy ( 4-Bx) • Menopause before 49 years
• Menopause after 52 years (2.4x) • Multiparity
• Obesity (2-Sx) • Smoking
• Nulliparity (2-3x)
• Diabetes (2.Bx)
• Insulin resistance
• Estrogen secreting ovarian tumors
• Polycystic ovarian syndrome (PCOS)
• Tamoxifen therapy for breast cancer
• Lynch syndrome

A. Grade (G) or Degree of Differentiation

G1 Well differentiated ,; 5% solid non-glandular, non-squamous components
G2 Moderately differentiated 6-50% solid non-glandular, non-squamous components
G3 Poorly differentiated >50% solid non-glandular, non-squamous components

Prototype • Endometrioid • Serous, clear cell

Typical Patient • Peri- or early postmenopause • Late postmenopause
BackgroundEndometrium • Hyperplastic • Atrophic
Grade • Low • High
Estrogen Dependence • Dependent • Non-dependent
Estrogen Receptors • Usually positive • Negative
Prognosis • Better • Poorer

C. Molecular Classification of Endometrial Cancer

MUTATION SURROGATE MARKER SURROGATE MARKER
PROFILE
Ultramutated
I (Genetic)
• POLE mutation
I (IHC)
• None available
Hypermutated • MSI-H • MMR-D
Copynumber high • TPS3 mutation • PS3 abn
Copy number low • Absence of other markers • Absence of other parkers (p53 wt)
abn indicatesabnormal:IHC,immunohistochemistry; MMR-D,
mismatchrepairdeficient;MSI-H,microsatellite
instability-high;
POLE,polymeraseE; wt, wild-type.
Source:Soslowet al. IntJ GynPath. 2018
II. MANIFESTATIONS
• Primary symptoms of endometrial carcinoma:
0 Postmenopausal/perimenopausal bleeding
0 Abnormal premenopausal bleeding
• Most frequent site of distant metastasis of adenocarcinoma of the endometrium are the
lungs, retroperitoneal nodes, and abdomen
504
F/GO Sta.ain.a Classification for Endometrial Cancer•
Stage I Gl GZ G3 Tumor confined to the corpus uteri
IA No or less than half of the myometrial invasion
1B Invasion equal to or more than half of the myometrium
Stage II Gl GZ G3** Tumor invades the cervical stroma, not extending beyond the uterus
Stage III Gl GZ G3 Local and/or regional spread of the tumor
IIIA Tumor invades serosa of the corpus uteri and/or adnexae
11IB Vaginal and/or parametrial involvement
me Metastasis to the pelvic and/or para-aortic lymph nodes
IIICl Positive pelvic lymph nodes
IIICZ Positive para-aortic LN with or without positive pelvic lymph nodes
Tumor invades bladder and/or bowel mucosa, and/or distant
Stage IV Gl GZ G3
metastasis
IVA Tumor invasion of bladder and/or bowel mucosa
Distant metastases, including intra-abdominal metastases and/or
IVB
inguinal lymph nodes
'Positivecytologyhas to be reportedseparatelywithoutchangingthe stage
"Endocervicalglandularinvolvement shouldbe consideredas Stage 1 and no longeras stage II

Ill. DIAGNOSIS
• Biopsy of the endometrium
• WHO histological classification of tumors of the uterine corpus:
• Endometrioid adenocarcinoma
• Endometrioid adenocarcinoma with squamous differentiation
• Clear cell carcinoma
• Serous carcinoma
• Secretory carcinoma
• Mucinous carcinoma
Squamous carcinoma
0 Mixed carcinoma
• Undifferentiated carcinoma
• Carcinosarcoma

IV.MANAGEMENT
• Surgery is the primary treatment modality for patients with endometrial carcinoma
• Standard management of endometrial cancer includes the following surgical procedures:
• Peritoneal fluid cytology (PFC)
Extrafascial hysterectomy (EH)
Bilateral salpingo-oophorectomy (BSO)
Bilateral pelvic lymph node dissection (BLND)
Para-aortic lymph node sampling (PALS)
• Exceptions to surgical approach
Poor surgical risk: should undergo primary complete radiotherapy with or without

·:
chemotherapy
Non-resectable disease: should undergo primary complete radiotherapy with or
without chemotherapy
• Well-differentiated lesion and contraindications to anesthesia and unsuited for
radiotherapy - may use high-dose progestins ■·
• Patients desirous of future fertility who have all the following criteria:
• Well-differentiated tumor (Grade 1, endometrioid type)
• No myometrial, cervical, adnexal, parametrial and vaginal involvement on MRI
• No suspicious retroperitoneal lymph nodes or no evidence of lymph node metastasis
• Negative PFC
• No lymphovascular space invasion (LVSI)
• No contraindications for medical management
505
 STAGE I
I SURGICO-PATHOLOGIC
STAGING I ADJUVANTTREATMENT

Surgery: PFC, EHBSO, BLND ± PALS (indicated for Stage 1Band/orG3 tumors)

Gl, G2 Observe
IA
G3 Brachytherapy

Gl,G2 Brachytherapy
1B
G3 EBRT ± Chemotherapy*

Surgery: PFC, EHBSO, BLND, PALS

Gl, G2 Brachytherapy

G3 EBRT ± Brachytherapy ± Chemotherapy

STAGE II
Surgery: PFC, RHBSO, BLND, PALS
Observe, unless with poor surgico-
Gl, G2, G3
pathologic factors

STAGE III Surgery: PFC, EHBSO, BLND, PALS± Tumor Debulking

IIIA Gl, G2, G3 Chemotherapy+ EBRT

IIIB Gl,G2,G3 Chemotherapy+ EBRT ± Brachytherapy

IIIC1 Gl, G2, G3 Chemotherapy+ EBRT ± Brachytherapy

IIICZ Gl,G2,G3 Chemotherapy+ EFRT ± Brachytherapy

STAGEIV Surgery: EHBSO ± Tumor Debulking

IVA Gl,G2,G3 Chemotherapy+ EFRT ± Brachytherapy

IVB Gl,G2,G3 Chemotherapy+ EFRT ± Brachytherapy

'Chemotherapy:Platinum-based(e.g., Carboplatin+ Paclitaxel)
EBRT:Externalbeam radiotherapy;EFRT:Extendedfieldradiotherapy

NOTE:For tumorswithpoor histologictype (i.e. serous, clear cell, carcinosarcoma).extended surgicalstaging in

the formof Peritonealfluidcytology(PFC), EHBSO,lnfracolicOmentectomy(10),Random PeritonealBiopsy(RPB),
BLND,PALS± TumorDebulkingis performed.

Conservative Mana_qement o{Endometrial Adenocarcinoma G1:

• Progestational agents:
, Megestrol acetate OR
' Medroxyprogesterone acetate OR
' LNG-IUS plus an oral progestin
• Monitoring:
'Perform endometrial biopsy every 3 months of progestin treatment. No response after
6 months of therapy means treatment failure.
, For patients who have complete response, an endometrial biopsy should be repeated
after 3 months. After 2 consecutive negative biopsies, pregnancy must be pursued in
consultation with an infertility specialist.
'After completion of childbearing plans, definitive staging surgery must be performed

V. FOLLOW-UP
• Every 3-6 months for 2 years, then every 6-12 months thereafter
• Pap smear is not routinely indicated
• PET-CT Scan, CT Scan, MRI and/or Bone Scan if suspicious for tumor recurrence
• Annual chest x-ray is not recommended for early detection of recurrent disease in
asymptomatic patients
• Serum CA-125 monitoring every 3 months for selected patients (i.e. advanced stages
[Stages III-IV], poor histologic type [serous or clear cell] and/or an elevated pre-
treatment CA-125 level)
506
 SECTION FOUR
OVARIAN CANCER
ETIOPATHOGENESIS
• Ovarian cancer is the second most common malignancy of the female lower genital tract
• Most frequent cause of death from gynecologic neoplasms
• Major contributing factor to the high death rate is the frequent detection of the disease
after metastasis
• Theories on pathogenesis:

• Lesions in the fallopian tube called serous intraepithelial

Fallopian tube as origin carcinomas (STICs) are precursors for most high-grade
serous epithelial ovarian cancers

Incessant ovulation • Ovarian epithelium is damaged during ovulation and

repair makes cells susceptible to mutations

Gonadotropin • Stimulatory effects of FSH and LH promote growth,

increased cell divisions, and mutations
• Structures in the paraovarian and paratubal areas
Extrauterine Miillerian (endosalpingiosis, endometriosis and endocervicosis)
Epithelium may develop into epithelial ovarian tumors or peritoneal
carcinoma

I. TYPESOF OVARIANCARCINOMAS
EXPLAININGTUMORHETEROGENEITY
CHARACTERISTIC
I TYPE 1
I TYPE 2
• 25% of ovarian malignancies • 75% of ovarian malignancies
Epidemiology
• 10% of deaths • 90% of deaths
• Low-grade serous • High-grade serous
• Low-grade endometrioid • High-grade endometrioid
Histology • Clear cell • Undifferentiated
• Mucinous • Carcinosarcoma
• Brenner • Transitional cell
• Cystadenoma
• Serous tubal intraepithelial
Early lesion • Borderline Cystadenoma
carcinoma (STIC)
• Endometriosis
Morphological
• Identified • Not identified
precursors
Presentation
and transition to • Indolent, slow, gradual • Rapid growth, abrupt
malignancy
• Multifocal distribution, • Mesothelial lined surfaces of
Spread pattern distant recurrence, systemic the ovary, fallopian tube, and
spread peritoneum
Stage of diagnosis • Early • Advanced
Prognosis • Good • Poor
• Genomic stability

■
• Genomic instability
• Frequent mutations: KRAS,
Genomic profile and • p53 mutation,
BRAF,ERBBZ,PTEN,
mutations BRCAl/2 inactivation,
B-catenin, PIK3CA,CTNNBl,
CCNEl multiplication
ARIDlA
Sources:Rescigno et al. BiomedResInt,2013.
Aggarwalet al.The Obstetrician
andGynaecologist, 2016.
507
II. WHO HISTOLOGICALCLASSIFICATIONOF TUMORS OF THE OVARY
• Serous • Clear cell (Mesonephroid)
Epithelial (65%) • Mucinous • Brenner
• Endometrioid

• Primitive (dysgerminoma, endodermal sinus tumor)

Germ Cell (6%)
• Teratoma
• Granulosa cell tumor
Sex Cord (<0.01%) • Thecoma, fibroma
• Sertoli-Leydig
Germ Cell-Sex Cord(< 0.01%) • Gonadoblastoma
• Tumors of rete ovarii • Large cell carcinoma
Miscellaneous
• Small cell carcinoma • Extrarenal Wilm tumor

Ill. EPITHELIALTUMORS (most common)

Serous Tumors
• Most frequent ovarian epithelial tumors
• Resembles fallopian tubes

• Epithelial cells filled with mucin

Mucinous Tumors
• Resembles endocervix/gastrointestinal tract
• Contains cell with abundant glycogen (hobnail cells)
Clear Cell
• Associated with diethylstilbestrol [DES) exposure
Endometrioid • Epithelial cells resembling the endometrium
Brenner • Resembles the transitional cells of the urinary bladder

IV. RISK FACTORSOF OVARIANEPITHELIALCARCINOMA

INCREASES THE RISK I DECREASES THE RISK
• Age • Nulliparity • Breastfeeding
• Diet • Ovulation and • Oral contraceptive pills
• Family history ovulatory drugs • Pregnancy
• Industrialized country • Talc (controversial) • Tubal ligation or opportunistic
• Infertility salpingectomy, and hysterectomy,
with ovarian conservation
Source:HerbstAL.AmJ ObstetGynecol.1994

508
MANIFESTATIONS AND DIAGNOSIS
I. MANIFESTATIONS
• Early disease is nearly always almost asymptomatic
• Vague pelvic pressure
Signs & Symptoms
• Abdominal fullness and bloating
(non-specific)
• Dyspepsia
• Advanced disease may present with ascites
Abdominopelvic Exam • Predominantly solid, fixed, irregular abdominopelvic mass
findings with or without ascites

II. DIAGNOSTIC TOOLS

Pelvic Ultrasound with
Dopplers using the • Primary tool for evaluation of a pelvic mass
IOTA-ADNEX* Models

PET-CT Scan, MRI or CT • Determine origin of the tumor, extent of the disease and
Scan with contrast probability of achieving optimal cytoreductive surgery
• 80% of patients with epithelial ovarian cancer have elevated
Tumor markers
CA-125
'InternationalOvarianTumorAnalysis-Assessment
of DifferentNEoplasiasin the adneXa(IOTA-ADNEX)

III. WHO CLASSIFICATION OF OVARIAN TUMORS

TYPE
I AGE I TUMOR
MARKERS
I HISTOLOGY

• Serous (low grade or • Brenner

high grade) • Transitional
• CA-125
• Mucinous • Epithelial-stromal
Epithelial • Older • CEA
• Endometroid • Mixed
• CA 19-9
• Clear cell
( mesonephroid)
• Dysgerminoma • Embryonal carcinoma
• LOH
• Endodermal sinus • Polyembryoma
Germ Cell • Young • ~-hCG
• Immature teratoma • Mixed
• AFP
• Choriocarcinoma • Mature teratoma
• lnhibin • Granulosa cell • Thecoma
Sex Cord • All
•AMH • Sertoli-Leydig • Fibroma

IV. COMPLETE SURGICALSTAGING

• Staging is surgical with an objective of optimal cytoreductive surgery (i.e. zero residual tumor)
• Staging:
0 Laparotomy: midline vertical incision
0 Peritoneal fluid cytology (PFC)
0 Systematic exploration of the abdominopelvic cavity
Total hysterectomy with bilateral satpingo-oophorectomy (THBSO);
Unilateral salpingooophorectomy (USO) with frozen section (FS)
0 lnfracolic or infragastric omentectomy (10)
0 Lymph node dissection (pelvic and para-aortic)
0 Random biopsy of abdominopelvic peritoneum, adhesions and suspicious areas
0 Tumor debulking
Appendectomy if mucinous histology or if the appendix is grossly involved with tumor

V. CRITERIA FOR FERTILITY-SPARING SURGERY(FSS)

• Stage !A-IC • Grade 1 or 2 disease
• Good histologic type • Desirous of future fertility
509
VI.FIGOSfAGINGCLASSIFICATION
FOROVARIAN,
FALLOPIAN
TUBEANDPERITONEAL
CANCER
STAGE I LOCATION
I A
I B I C

• 1 or 2 ovaries or
FTs with any of
• 1 ovary or FT the following:
• 2 ovaries or FTs
only • Cl: surgical spill
• No tumor on
• No tumor on
ovarian or FT • CZ:ovarian
• Confined to ovarian or FT capsule or FT
surface
ovaries or surface
I fallopian tubes • No malignant
• No malignant serosa ruptured
cells in the before surgery or
(FT) cells in the tumor on ovarian
ascites or
ascites or
peritoneal surface
peritoneal
washings • C3:malignantcells
washings
in the ascites or
peritonealwashings
• 1 or 2 ovaries or
FTswith • Extension and/
• Extension to
• Pelvic extension or implants on
other pelvic
II (below pelvic the uterus and/
intraperitoneal
---
brim) or or FTs and/ or
tissues
• Primary ovaries
peritoneal cancer

•Ali:(+)
retroperitoneal
• Macroscopic • Macroscopic
LN metastases
peritoneal peritoneal
510mm
metastasis metastasis
in greatest
beyond pelvis,;; beyond pelvis
• Stage II PLUS dimension
2 cm in greatest > 2 cm in greatest
• Cytologically or
• Alii: (+) dimension, dimension,
histologically
retroperitoneal with or without with or without
confirmed
LN metastases positive positive
spread to the
> 10mm retroperitoneal retroperitoneal
III peritoneum
in greatest LNs LNs
outside the
dimension • Includes • Includes
pelvis and/or
extension of extension of
metastases to the • A2: (+) tumor to liver tumor to liver
retroperitoneal microscopic and/or spleen and/or spleen
LNs extrapelvic capsule without capsule without
(above the pelvic parenchymal parenchymal
brim) peritoneal involvement of involvement of
involvement+/- either organ) either organ)
positive retro-
peritoneal LNs
• Parenchymal
metastasis (liver
• Distant and/or spleen)
metastases & metastasis to
• Pleural effusion
IV excluding
with(+) PFC
extra-abdominal ---
peritoneal organs (including
surfaces inguinal LJ':!sand
LNs outside of the
abdominal cavity)

VII. MANAGEMENT
• First line post-operative/adjuvant management, if indicated, is usually platinum-based
chemotherapy± targeted therapy:

Epithelial Tumor • Paclitaxel + Carboplatin ± Bevacizumab

Germ Cell Tumor and
• Bleomycin + Etoposide + Cisplatin [BEP]
Sex-Cord Stromal Tumor
510
OVARIAN TUMOR: GERM CELL
I. ETIOPATHOGENESIS
• Most common ovarian malignancy in women< 30 years old
• Grow rapidly, usually unilateral, and are at stage lA at diagnosis (compared to epithelial
tumors)

GERM CELLTUMORS
25-25% of all ovarian tumors

BENIGN TUMORS ..
95% ----- MALIGNANT
~5%
Mostly benign cystic teratoma
(mature teratoma/ dermoid tumor)
....._.._ lk sac- endodermal
'- - chorfocarci
e-immatu

II. MANIFESTATIONS
• Pelvic pain due to rapid growth, hemorrhage, and necrosis
• Pressure symptoms on the bladder or rectum
• 85% will have abdominal pain and pelvic mass

III. DIAGNOSIS
GERM CELL TUMOR TUMOR
(MALIGNANT)
I HISTOLOGY

• Germ cells stroma infiltrated with

I MARKER

lymphocytes
Dysgerminoma • LDH
• 10% are bilateral
• Analogous to seminoma of the testes
Endodermal sinus tumor • Schiller-Duval bodies - numerous hyaline
• AFP
or Yolk sac tumor droplets
• Hemorrhagic
Choriocarcinoma • Highly malignant cytotrophoblast and • ~-hCG
syncytiotrophoblast (dimorphic pattern)
• Consists of immature embryonic structures
Immature teratoma • AFP
admixed with mature elements

IV.MANAGEMENT
• If fertility is desired: PFC, USO+ Complete Surgical Staging (IO, RPB, BLND,PALS)±
Tumor Debulking

■
• No desire for fertility: PFC, TAHBSO,JO, RPB, BLND,PALS± Tumor Debulking

511
OVARIAN TUMOR: SEX CORD
I. ETIOPATHOGENESIS
• Sex cord stromal tumors are functioning tumors meaning these tumors secrete either
estrogen (granulosa cell) or testosterone (Sertoli-Leydig)
• May manifest with symptoms attributable to the excess hormone production (i.e.
precocious puberty, abnormal uterine bleeding, virilizing symptoms)

I GRANULOSA CELL
TUMOR(75%)
• Sex Cord: Granulosa
I SERTOLI LEYDIG CELL
TUMOR
• Sex Cord: Sertoli
Component
• Strama: Theca • Strama: Leydig
• Granulosa cells have grooved "coffee
bean" nuclei and are arranged in small
Microscopic • Resemble fetal testes
clusters around a central cavity
(Call-Exner bodies)
• Functionally
Hormones • Functionally estrogenic
testosterogenic
• Virilization
• Premenarcheal: precocious puberty
• Hirsutism
Symptoms • Premenopausal: menstrual irregularities
• Temporal recession
• Postmenopausal: bleeding
• Deeper voice
• Desirous of pregnancy: PFC, USO+ Complete Surgical Staging
Management • Not desirous of pregnancy: PFC, THBSO,IO, RPB, BLND,PALS
± Tumor Debulking
Tumor marker • lnhibin, AMH

512
 SECTION FIVE
VULVAR CANCER
ETIOPATHOGENESIS
• Accounts for approximately 4%-5% of female genital tract malignancies
• Occurs less often than uterine, ovarian and cervical cancers
• More than 80% of patients are older than 50 years at the time of diagnosis
• 90% of primary vulvar malignancies is squamous cell carcinoma (SCCA)

CHARACTERISTIC
I TYPE! I TYPE II
Age group • 35-65 years of age • 55-85 years of age
• Human papillomavirus • Vulvar non-neoplastic
Etiology
(HPV) infection epithelial disorders (VNED)
• Lichen sclerosus
Precursor lesion • LGSIL-HGSIL(VIN 1-3) • Lichen planus
• Squamous hyperplasia
• Sexually transmitted
Other predisposing diseases (STDs)
• "Itch-scratch cycle"
factors • Low socioeconomic status
• Nicotine use
Somatic mutation --- • TP53
Source:Gershenson
et al. Comprehensive Gynecology,
8th Ed.2022
Alkatoutet al. Int J WomenHealth,2015.
II. RISK FACTORS
INCREASES THE RISK I DECREASES THE RISK
• Human Papilloma Virus infection • HPV vaccination
• Tobacco smoking • Prompt treatment of lichen sclerosus,
• Untreated vulvar dermatoses lichen planus and squamous hyperplasia
• Presence of anogenital warts • Cessation of smoking
• History ofvulvar atypia
• History ofpreinvasive disease or invasive
cancer of the cervix and/or vagina
• Alcohol consumption

CLINICAL MANIFESTATIONS
SYMPTOMS I SIGNS
• Long history ofvulvar pruritus • Vulvar lump or mass
• Vulvar bleeding ° Fungating or ulcerated
• Vulvar discharge ° Fleshy or warty
• Vulvar pain 0 Leukoplakic
• Dysuia • Palpable groin node(s)

·:
• Dyschezia • Leg edema
Source:Alkatoutet al. Int J WomenHealth,2015.
DIAGNOSIS
• Punch or incision biopsy at the peripheral edge of the tumor using a Tischler or Keyes ■·
biopsy instrument
0Include underlying stroma
0Avoid necrotic center of the tumor
• Pap smear and colposcopy to rule an associated lesion on the cervix and vagina
• Imaging: PET-CTScan, CT Scan, MRI, ultrasound
• Endoscopy: cystoscopy, proctosigmoidoscopy
Source:CPGfor the Obstetrician-Gynecologist,
3rd Ed,SGOP,2019
513
WHO2020 Classification of Tumors of the Vulva
• Squamous cell carcinoma
HPV-associated
0

HPV-independent
0

NOS
0

Epithelial tumors • Basal cell carcinoma

• Verrucous carcinoma
• Phyllodes tumor
Borderline
0

Malignant
0

• Adenocarcinoma of anogenital mammary-like gland

• Squamous cell carcinoma, NOS
• Adenoid cystic carcinoma
• Carcinoma, poorly differentiated, NOS
Bartholin gland • Adenosquamous carcinoma
lesions • Neuroendocrine tumor, NOS
• Myoepithelial carcinoma
• Epithelial-myoepithelial carcinoma
• Squamous cell carcinoma, HPV positive

• Germ cell tumor, NOS

Germ cell tumors
• Yolk sac tumor NOS
• Sweat gland adenocarcinoma
Apocrine adenocarcinoma
0

Eccrine adenocarcinoma
0

Other tumors Porocarcinoma, NOS

0

Adenoid cystic carcinoma

0

• Adenocarcinoma, intestinal type

• Melanoma
• Sarcoma
Source: Female GenitalTractTumors,fromthe WHOClassificationof TumorsSeries, 5th Ed, 2020.

FIGO2021 Staging for Carcinoma of the Vulva

STAGE I DEFINITION
I • Tumor confined to the vulva
IA • Tumor size ,;2 cm and stromal invasion ,;1 mm'
1B • Tumor size >2 cm or stromal invasion >l mm'
• Tumor of any size with extension to lower one-third of the urethra or vagina or
II
anus, with negative nodes
• Tumor of any size with extension to upper part of adjacent perinea! structures,
III
or with any number of nonfixed, non-ulcerated lymph node
• Tumor of any size with disease extension to upper two-thirds of vagina, bladder
IIIA
mucosa, rectal mucosa, or regional lymph node metastases ,;5 mm
IIIB • Regionals lymph node metastases >5 mm

me • Regionals lymph node metastases with extracapsular spread

• Tumor of any size fixed to bone, or fixed, ulcerated lymph node metastases, or
IV
distant metastases

IVA • Disease fixed to pelvic bone, or fixed or ulcerated regionaJbJymph node metastases

IVB • Distant metastases

'Depth of invasionis measured fromthe basement membraneof the deepest, adjacent,dysplastic,tumor-freerete
ridge (or nearest dysplasticrete peg) to the deepest pointof invasion.
'Regional refers to inguinaland femorallymphnodes.
Source: Olawaiyeet al. FIGOStagingfor Carcinomaof the Vulva,2021.
514
MANAGEMENT
STAGE I PRIMARY TREATMENT
I ADJUVANTTREATMENT
IA • Radical local excision (RLE)
• RLE with ipsilateral groin
node dissection
or
• RLE with bilateral groin node • Concomitant chemoradiation (i.e.
1B dissection (BGND) if with any external beam radiotherapy to the
of the following: vulva, groin, pelvis with chemotherapy)
0 Lesion within 1.0 cm from if with any poor surgicoprognostic
the midline structures factors:
0 Involvement of labia minora ' Positive surgical margins
, Gross surgical margins < 1.0 cm
• RLE with BGND
, Microscopic surgical margins< 5 mm
or
' Thickness > 5 mm
• RLE with sentinel lymph node
, Positive lymphovascular invasion
(SLN*) dissection; perform
(LVSI)
II groin node dissection if SLN is
positive for tumor
or
• Radical vulvectomy (RV) with
BGND
III
(Tumor
• Concomitant chemoradiation (i.e.
resectable
• RVBGND external beam radiotherapy to the
without
vulva, groin, pelvis with chemotherapy)
requiring
stoma)
III
(Tumor • Concomitant chemoradiation
resectable (i.e. external beam
but radiotherapy to the
• Possible surgical resection
requiring vulva, groin, pelvis with
stoma) chemotherapy± interstitial
brachytherapy)
IVA
• Systemic chemotherapy ±
IVB ---
radiotherapy
Forpatientswhoare poorsurgicalrisk:concomitantchemoradiation
(i.e.externalbeam radiotherapyto the vulva,
groin,pelviswithchemotherapy± interstitialbrachytherapy)

'Criteriafor SentinelLymphNode(SLN)Mapping:
1) Tumorsize,; 4 cm
2) > 1 mminvasion
3) Noclinicallysuspiciouslymphnodes
4) Nopreviousgroinnodedissection
5) Nopriorgroinirradiation
6) Notfor multifocaldisease
7) Notgrosslyinflamedprimarytumor
8) Notfor recurrentdisease
Sources:ClinicalPracticeGuidelines,SGOP,20181
van der Zee et al. J ClinOneal,2008. : :

515
REFERENCES
l.Abhatla N,Aoki D, Sharma D, etal. Cancer of the cervix uteri. IntJ Gynaecol Obstet 2018;143:22-36; Corrigendum to "Revised
FIGO staging for carcinoma of the cervix uteri". Int J Gynaecol Obstet 2019;147:279-280.
2.Aggarwal IM, Lim YH and Lim TYK.The Fallopian Tube as the Origin of Non-Uterine Pelvic High-Grade Serous Carcinoma.
The Obstetrician & Gynaecologist 2016:18:143-152.
3.Alkatout I, Schubert M,Garbrecht N,Weigel MT,Jonat W, Mundhenke C and Gilnther V.Vulvar Cancer: Epidemiology,Clinical
Presentation and Management Options. Int J of Women's Health. 2015:7:305-313.
4.Emons G, Beckmann MW, Schmidt D, Mallmann P and for the Uterus Commission of the Gynecological Oncology Working
Group (AGO). New WHO classification of endometrial hyperplasias. Geburtsh Frauenheilk 2015 Feb:75(2):135-136.
5.Fontham ETH, Wolf AMO, Church TR. Etzioni R. Flowers CR, Herzig A, et al. Cervical Cancer Screening for Individuals at
Average Risk: 2020 Guideline Update from the American Cancer Society. CA CANCERJ CLIN 2020;70:321-346.
6.Gershenson OM, Lentz GM, Valea FA, Lobo RA. Comprehensive Gynecology. 8th Ed. Philadelphia: Elsevier; Inc.; 2022.
7.Handisurya A, Schellenbacher C, Kirnbauer R. Diseases caused by human papillomaviruses (HPV). JDDG 2009;7:453-466.
8.Herbst AL. The epidemiology of ovarian carcinoma and the current status of tumor markers to detect disease. Am J Obstet
Gynecol.1994;170(4):1099-1105
9.Lobo RA, Gershenson OM, Lentz GM, Valea FA.Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
10. Melnikow J, Henderson JT.Burda BU,Senger CA,Durbin S, Souls by MA.Screening for Cervical Cancer With High•Risk Human
Papillomavirus Testing: A Systematic Evidence Review for the U.S. Preventive Services Task Force. Evidence Synthesis No.
158. AHRQ Publication No. 17-05231-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2018.
11. Nayar Rand Wilbur DC.The Pap Test and Bethesda 2014. Acta Cytologica 2015;59:121-132.
12. Olawaiye AB, Cotler J, Cuello MA, Bhatia N, Okamoto A, Wilailak S et al. FIGO Staging for Carcinoma of the Vulva: 2021
Revision. Int J Gynecol Onstet. 2021:155;43-47.
13. Perkins RB, Guido RS, Castle PE, Chelmow D, Einstein MH, Garcia F,et al. 2019 ASCCP Risk-Based Management Consensus
Guidelines for Abnormal Cervical Cancer Screening Tests and Cancer Precursors. J Low Genit Tract Dis 2020;24: 102-131.
14. Rescigno R. Cerillo I, Ruocco R, Condello C, De Placido Sand Pensabene M. New Hypothesis on Pathogenesis of Ovarian
Cancer Lead to Future Tailored Approaches. Biomed Research International Volume 2013: Article ID 8522839;13 pages.
15. Schorge JO, Modesitt SC, Coleman RL, Cohn DE, Kauff ND, Duska LR, Herzog TJ. SGO White Paper on ovarian cancer:
etiology, screening and surveillance. Gynecol Oneal. 2010
16. Society of Gynecologic Oncologists of the Philippines (SGOP) Clinical Practice Guidelines for the Obstetrician•Gynecologist.
3rd Ed.; July 2019.
17. Society of Gynecologic Oncologists of the Philippines (SGOP) Clinical Practice Guidelines. 8th Ed.; July 2018.
18. Soslow RA, Tornos C, Park KJ, Malpica A. Matias-Guiu X., Oliva E., et al.. Endometrial Carcinoma Diagnosis: Use of FIGO
Grading and Genomic Subcategories in Clinical Practice: Recommendations of the International Society of Gynecological
Pathologists. Int J Gynecol Pathol Jan 2019:38(1) Suppl 1: S64-S74.
19. Union for International Cancer Control (UCC).Bth edition of the UICCTNM classification of malignant tumours (2016).
20. WHO Classification of Tumours Editorial Board. Female Genital Tract Tumours. Lyon (France). International Agency for
Research on Cancer, 2020. (WHO Classification of Tumours series, 5th ed: vol 4). https://publications.iarc.fr/592.
21. van der Linden M, Meeuwis KAP,Bulten J,Bosse T, van Poelgeest MIE and de Hullu JA. Paget Disease of the Vulva. Critical
Reviws in Oncology/Hematology. 2016:101;60-74.
22. Van der Zee AG, Oonk MH, De Hullu JA, Ansink AC, Vergote I, Verheijen RH, et al. Sentinel node dissection is safe in the
treatment of early stage vulvar cancer. J Clin Oncol 2008;26(6):884-9.

516
GESTATIONAL
TROPHOBLASTIC
DISEASE
ANDNEOPLASIA
 SECTION ONE
OVERVIEW OF GESTATIONAL TROPHOBLASTIC DISEASES

GESTATIONAL TROPHOBLASTIC DISEASES (GTD)

• Comprise a group of lesions due to abnormal proliferation of trophoblast of the placenta (i.e.,
maternal lesions arise from fetal tissue, not maternal), ranging from benign to malignant
• It has a varying predilection toward local invasion and distant metastasis
• Trophoblast produces human chorionic gonadotropin (hCG), thus the measurement of
this hormone is essential for GTD diagnosis and management

I. CLINICALCLASSIFICATION
HYDATIDIFORM MOLE I GESTATIONAL TROPHOBLASTIC
NEOPLASIA (GTN)*
• Invasive mole**
• Complete hydatidiform mole • Choriocarcinoma
• Partial hydatidiform mole • Placental site trophoblastic tumor (PSTT)
• Epithelioid trophoblastic tumor (ETT}
'Malignantformsof GTDare termed GTN. Otherterms for GTNare malignantgestationaltrophoblasticdisease
and persistentgestationaltrophoblasticdisease.
"Invasive moleis deemed malignantdue to its markedpenetrationintoand destructionof myometriumand its
abilityto metastasize.
Source:WHOClassificationof GTD

II. PATHOLOGY
• Most GTD produces the beta-subunit of human chorionic gonadotropin (P-hCG)
• Assessment of DNA content enhances the diagnostic accuracy of histologic diagnosis
• With excess paternal genes, there is excessive placental or trophoblastic proliferation
(because paternal genes have more control over placental growth)

III. CRITERIAFOR DIAGNOSISOF GESTATIONALTROPHOBLASTICNEOPLASIA (GTN}

• Half of GTN follow hydatidiform mole
• The 4 tumor types (see table above) are histologically distinct, but are usually initially
diagnosed solely by persistently elevated serum P-hCG levels because tissue is
infrequently available for study

FIGO Criteria for Diagnosis ofGTN

• Plateau of serum P-hCG level ( +/-10%) for 4 measurements during a period of ~3 weeks
(days 1, 7, 14, 21)
• Rise of serum P-hCG level > 10% on ~3 weekly consecutive measurements, during a period
of~Z weeks (days 1, 7, 14)
• Serum P-hCG level remains detectable for ~6 months
• Histoiogic criteria of choriocarcinoma

519
■
 SECTION TWO
BENIGN GESTATIONAL TROPHOBLASTIC DISEASES

HYDATIDIFORM MOLE (MOLAR PREGNANCY)

• Characterized histologically by abnormalities of the chorionic villi, consisting of various
degrees oftrophoblastic proliferation & edema ofvillous stroma
• Non-viable, genetically abnormal pregnancy due to an excess expression of paternal
genes which causes varying degrees of trophoblastic proliferation and vesicular swelling
of placental villi
• Arise from chromosomally abnormal fertilizations with excessive placental, and little or
no fetal, development

I. ETIOPATHOGENESIS
• H-mole is categorized as complete or partial mole
• They occur after an aberrant fertilization

A. Complete H-mole (CHM) versus Partial H-mole (PHM)

I COMPLETE H-MOLE
(DIANDRIC, DIPLOIDY)
I PARTIAL H-MOLE
(DIANDRIC, TRIPLOIDY)
• 1 maternal (23X) and 2 paternal
• Paternal chromosome only plus
chromosomes (23X, 23Y)
empty ovum
• Maternal chromosome gives rise
• Gives rise to generalized
to fetal component
Pathogenesis swelling of placental villi
• Paternal chromosome causes
with marked trophoblastic
focal swelling of placental villi
proliferation and absent fetal
and milder form oftrophoblastic
component
invasion
Homozygous

~--0--®)
Triploid partial mole

Empty ovum
Heterozygous
complete mole

~
23, Y

Oispermy

Illustration ~

• Most (80%) are homozygous

46XX resulting from duplication
of the haploid genome of
• Usually result from fertilization of
a single sperm following
a normal ovum by two sperm
fertilization of an ovum
• May be 69XXX,69XXY,or 69XYY
• The remaining arise by
dispermic fertilization of an
ovum and may be 46XX or 46XY
• 46XX or 46XY • 69XXX or 69XXY or 69XYY
Karyotype
• Diploid • Triploid
Preliminary
• Molar gestation • Missed abortion
diagnosis

520
 B. Risk Factors
RISK
I REMARKS
Extremes in • Two-fold risk for those <15 years old, 36-40 years old
maternal age • Ten-fold risk for those >40 years old
Paternal age • >45 years old increases risk for complete but not partial mole
OB history • Previous molar pregnancy
Racial factors • Asians, Hispanics, American-Indians
Diet and Nutrition • Decreased dietary carotene & animal fat
'Strongest riskfactorsare age and a priorhydatidiform
mole

II. MORPHOLOGY
AND MANIFESTATIONS

I COMPLETE H-MOLE PARTIAL H-MOLE

(DIANDRIC, DIPLOIDY) I (DIANDRIC, TRIPLOIDY)
Gross Morphol~gy
• Absent • May be present
Embryo-Fetus
• No FHT • May detect FHT depending on AOG
• Presence of placenta-like tissues
Gross vesicles • Large vesicles with admixed vesicles
Histologie Morphology
• Presence of large and regularly-
Villi • Edematous
sized villi
Trophoblastic • Moderate to severe • Focal, slight to moderate
proliferation • Marked trophoblastic atypia • Mild trophoblastic atypia
Blood Vessels • Present • Absent
Fetal Components • Absent • Present
p57K/PZ
• Negative • Positive
immunostaining
- ,,
Manifestations ,,
Common • Vaginal bleeding (most common) or amenorrhea
presentations • Positive pregnancy test

Uterine size • Larger than AOG • Same size or smaller than AOG
13-hCGLevel • >100,000 mlU/mL • <100,000 mlU/mL
Theca Iutein • Common (25-30%): due to LH,
• Rare
cysts FSH stimulation
• Hyperemesis, preeclampsia: due
to high 13-hCG
• Hyperthyroidism: due to
Medical thyrotropin-like effects of the
• Rare
complications 13-hCG
• Respiratory insufficiency: due to
trophoblastic deportation
• DIC:from profuse vaginal bleeding
Malignant
• 15-25% (higher) • 0.4-5.0%
transformation
Source:E1felPJ,et al. Gynecotog,c 200611
Cancer;

521
III. DIAGNOSIS
A. Serum Jl-hCGMeasurements
0 In complete molar pregnancy, Jl-hCGare elevated (more marked elevation in those
with more advanced moles)
0 In partial moles, Jl-hCGmay be significantly elevated, but more commonly
concentrations fall into ranges expected for gestational age (see below)

Expected p-hCG Levels in Pregnancy (The R Generation Study)

GESTATIONAL GESTATIONAL
AGE
I MEDIAN (RANGE)
I AGE
I MEDIAN (RANGE)

<9weeksAOG 59,973 (455 - 142,584) 16weeksAOG 29,614 (7,512 - 132,084)

9weeksAOG 75,494 (22,655 - 129,909) 17weeksAOG 24,426 (5,637 - 151,558)
10weeksAOG 74,655 (16,080 · 163,393) 18weeksAOG 20,693 (3,822 - 75,993)
11 weeksAOG 62,493 (10,340 - 187,852) 19weeksAOG 17,609 (3,895 - 90.628)
12weeksAOG 56,004 (8,105 · 164,125] 20weeksAOG 17,354 (3,128 · 78,841)
13weeksAOG 52,377 (4,618 - 166,478) 21 weeksAOG 15,088 (1,542 · 73,485)
14weeksAOG 47,267 [5,925 - 144,054) 22weeksAOG 16,174 (2,559 - 86,541)
15weeksAOG 37,303 (4,834 · 122,037) 23weeksAOG 12,415 (1,957 - 65,192)
Korevaaret al. The R GenerationStudy,2015

8. Sonography (Ultrasound)
0 Mainstay oftrophoblastic disease diagnosis (but not all cases are confirmed initially)
0 Most accurate non-invasive imaging modality
0 Most common mimics: incomplete or missed abortion
I FlNrnNGS
• Snowstorm-like pattern: echogenic uterine mass with numerous
Complete
anechoic cystic spaces (grape-like or hydropic villous change)
mole
• No fetus or amniotic sac seen
Partial • Thickened, multicystic placenta along with a fetus or at least fetal tissue
mole

C. Histologic Diagnosis
0 Provides a definitive diagnosis
0 lmmunostaining with P57KIP2: protein product of paternally imprinted but
maternally expressed gene CDKNIC
• Negative in CHM
• Positive in PHM
° Karyotyping (diploid, triploid)

D. Other Diagnostic Tests

° CBCwith platelet, differential counts
0 Liver function test: ALT,AST
0 Renal function test: BUN,creatinine
0 Thyroid function test: TSH, FT4, FT3
0 Urinalysis
° Chest X-ray

522
IV. MANAGEMENT

Suction • Preferred treatment, regardless of uterine size

curettage • Cervix is dilated to allow insertion of a suction curette
TAHBS ± BO with • For those with completed family size
mole in-situ • Decreases risk for local invasion

B. Chemoprophylaxis
, First line: methotrexate (second line: actinomycin DJ
' Given to patients with high risk for persistent disease & with the following features:
• Maternal age ;,40 years
• Uterine size larger than gestation by >6 weeks
• Serum f3-hCGtiter ;,100,000 mlU/mL
• Theca lutein cyst(s) ;,6 cm
• Medical complication arising from increased trophoblastic proliferation (e.g.
preeclampsia, thyrotoxicosis, DIC, pulmonary insufficiency)
• Recurrent H. mole
• Documented H. mole with a coexisting normal twin (given after delivery of the twin)
' May be given for those with probable poor compliance to follow up

C. Follow-up
• 1 week after surgical evacuation
Post-evacuation
• Every 2 weeks until f3-hCGbecomes normal for 2 consecutive tests
f3hCGmonitoring
• Every 1 month for first 6 months
• Avoid pregnancy during monitoring period
Follow-up advice • Ideal to use low-dose OCP for contraception
• Pregnancy allowed 6 months after normal f3hCG
• Do early ultrasound to rule out molar pregnancy
For succeeding
• Perform quantitative serum f3-hCG6 weeks postpartum
pregnancies
• Placenta submitted for histopathologic exam
Source:PSSTDCPG,2016

523
■
 SECTION THREE
GESl'.AlilONAL TROPHOBLASTIC NEOPLASIA (GTN)

INVASIVE MOLE AND CHORIOCARCINOMA

• Both are characterized by high levels of ~-hCG (as opposed to PSTT and ETT)
• Half of GTN arise from molar pregnancies

I. ETIOPATHOGENESISAND PATHOLOGY

I INVASIVE MOLE I CHORIOCARCINOMA

• Most common
trophoblastic neoplasms
that follow hydatidiform
Description
moles (H. moles)
• Almost all arise from
partial or complete moles
• A hydatidiform mole that
has penetrated or invaded
into the myometrium
and/or has produced
metastases
Pathogenesis
• Characterized by
extensive tissue invasion
of the myometrium by
trophoblast and whole
villi
• Villi and trophoblasts
are seen within the
Pathology• myometrium
• Locally aggressive, but
less prone to metastasize
neoplasiasis usuallymade by persistentlyelevatedserumB-hCGlevelswithoutconfir•
'Diagnosisof trophoblastic
mationbytissuestudy. Clinicalstagingis assignedwithoutregardto histologicalfindings,even ifavailable
• Most common type of trophoblastic
neoplasm to follow a term pregnancy or a
miscarriage
• Etiology of malignant transformation is
still unknown
• May arise from any type of pregnancy
(even in a normal pregnancy, there can
be choriocarcinoma; unlike invasive mole
which only arises from an H. mole)
• Usual antecedent pregnancy is an H. mole
(50%)
• Cancer composed oftrophoblast, which
is the most invasive cell known in human
physiology
• Pure epithelial tumor composed of
syncytiotrophoblastic & cytotrophoblastic
cells (i.e. dimorphic pattern)
• Presents as necrotic hemorrhagic masses
or nodules in the uterus
• Microscopically, there is excessive
trophoblastic growth and lack of villous
architecture (unlike the invasive mole
wherein we can still see the villous
structures)

II. MANIFESTATIONS
• Persistent or irregular vaginal bleeding after a molar pregnancy (most common
presentation)
• Failure of uterine involution
• Signs and symptoms which may be referrable to the site of metastases
Lung: hemoptysis, dyspnea
0 Brain: headache, loss of consciousness, seizures
0 Gastrointestinal: melena, acute abdomen, abdominal pain
• Manifestations may be seen immediately or after years of antecedent pregnancy
• Metastasis is via the hematogenous route
• Most common site of metastasis: lungs which show "cannonball" lesions on radiologic
imaging

524
III. DIAGNOSIS
• High index of suspicion
• Histopathology is not necessary for the diagnosis of GTN
• Clinical manifestations (e.g., abnormal bleeding or amenorrhea, pelvic pain)
• High levels of P-hCG
• Ultrasonography with Doppler studies
• Histopathologic findings if hysterectomy is performed

IV. FIGO STAGINGAND DIAGNOSTICSCORINGSYSTEM FOR GTN

• All patients must be staged using the FIGO 2000 Staging System and scored using the
WHO Prognostic Scoring System

A. Anatomical Staging
STAGE
I EXTENT
I • Disease confined to the uterus
II • GTN extends outside the uterus but is limited to the genital
structures (adnexae, vagina, broad ligament)

III • GTN extends to the lungs with or without genital tract involvement

IV • All other metastatic sites

B. Modified WHO Prognostic Scoring System

SCORES
I 0 I 1 I 2 I 4

Age <40 .>40 --- ---

Antecedent
pregnancy
Mole Abortion Term ---
Interval months
from index <4 4-6 7-12 >12
pregnancy
Pretreatment
1,000 to 10,000 to
serum 13-hCG <l,000 .>100,000
<10,000 <100,000
(mJU/mL)
Largest tumor
size (including <3 cm 3-4cm ;,S cm ---
uterus)
Site of
metastasis* --- Spleen, kidney Gastrointestinal Liver, brain

Number of --- 1-4 5-8 >8

metastasis
Previous failed
chemotherapy
--- --- Single drug .>2 drugs

Interpretation:
• Lowrisk:<7 (suggests lowriskof resistance to single-agentchemotherapy)
• Highrisk:;, 7 (predictsa high riskof resistance to single-agentchemotherapy)

'Lung metastases do not confera score under the criteria"site of metastasis"

Source: FIGOCommitteeon GynecologicOncology.IntJ GynaecolObstet; 2009

525
■
VI. MANAGEMENT
A. Chemotherapy (cornerstone of treatment)
STAGE I MANAGEMENT
• Single agent chemotherapy (methotrexate or actinomycin DJ
I • ± hysterectomy

• Low risk: same as stage I

II • High risk: EMACO± hysterectomy
• Low risk: same as stage I
III • High risk: EMACO± hysterectomy
• EMACO
IV • ± hysterectomy
• ± irradiation
EMACO:
Etoposide,Methotrexate,
Actinomycin
D,Cyclophosphamide,
Vincristine

B. Consolidation Therapy
0Given after reaching normal P-hCG titers (i.e., ,;;S mIU/mL) to ensure eradication of
every viable trophoblast cells which may no longer be detected by the P-hCG assays
0Number of therapies:
• Low risk: 2 consolidation therapies
• High risk: 3 consolidation therapies

C. Surgery and Radiotherapy

0 Only adjunctive treatments

VII. FOLLOW-UPAFTER COMPLETIONOF TREATMENT

P-hCG • Every month for 6 months, then every other month for 6 months, then
monitoring every 3 months for the 2"' year, then every 6 months thereafter
• Avoid pregnancy until 2 years following completion of treatment
• Ideal to use low-dose OCP for contraception
Follow-up
• Transvaginal ultrasound every 6 months
advise
• Chestx-ray every year, if with residual lesions upon completion of
treatment
For • Perform serum ~-hCG 6 weeks postpartum
succeeding • Placenta submitted for histopathologic exam
pregnancies

526
PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT) AND
EPITHELIOID TROPHOBLASTIC TUMOR (ETT)
• Both have lower 13-hCGlevels compared to invasive mole and choriocarcinoma

I. ETIOPATHOGENESIS
• Usual antecedent pregnancy: term pregnancy
• Behavior is generally unknown due to rarity of conditions
PLACENTAL SITE EPITHELIOID
I TROPHOBLASTIC TUMOR I TROPHOBLASTIC TUMOR
• Rare tumor • Rare tumor
Pathogenesis • Arises from intermediate • Develops from chorionic-type
trophoblasts at the placental site intermediate trophoblast
• Main site of involvement is the
Pathology • Main site of involvement is the uterus
placental implantation site

II. MANIFESTATIONS
• Abnormal vaginal bleeding or manifestations referrable to the metastatic site
• Interval from the antecedent pregnancy is variable
• Serum 13-hCG:usually <2,000 mlU/mL, even with disseminated disease
• Staging: all patients are staged using the FIGO 2000 Staging System (the WHO prognostic
scoring system is not applicable)

III. MANAGEMENT
• Surgery is the primary mode of treatment
• Chemotherapy: EMACO
• Follow up: same as invasive mole and choriocarcinoma

REFERENCES
1. FIGO Committee on Gynecologic Oncology: Current FIGO Staging for Cancer of the vagina, fallopian tube, ovary, and
gestational trophoblastic neoplasia. Int) Gynaecol Obstet 2009 Apr;lOS(l):3-4
2. PhilippineSocietyfor the Study of TrophoblasticDiseases(PSSTD)Clinical PracticeGuidelinesfor the Diagnosisand
Managementof GestationalTrophoblasticDisease.3rd Ed.;2016,
3.Cunningham FG, Levene K, Bloom S, Spong C, Dashe), Hoffman 8, Casey 8. Williams Obstetrics. 25th Ed. New York:
McGraw-Hill Education Medical; 2018.
4. Lobo RA, Gershenson DM, Lentz GM,Valea FA.Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
5. EifelPJ,GershensonDM, KavanaghJI,SilvaEG.GynecologicCancer.New York:Springer-Verlag;2006:230.

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■
BOARD
CORRELATES
 SECTION
PREGNANCY AND PRENATAL CARE
Important values for jl-hCG
Naegele rule
Threshold of viability
Cardiovascular changes
Pulmonary changes
Gastrointestinal changes
Renal changes
Coagulation changes
Endocrine changes
Dermatologic changes
Nutritional requirements
Initial first visit and first
trimester tests
Second trimester tests
Third trimester
Components of biophysical
profile score
L/S ratio associated with
respiratory distress
ONE
OBSTETRICS
• 1,500 - 2,000 mlU/mL at 5 weeks AOG- gestational sac
• 5,000 - 6,000 mlU/mL at 6 weeks AOG- fetal heart rate motion
• 10,000 mlU at 10 weeks AOG- peak value
• Estimated date of conception
Month - 3, Day+ 7
• 280 days after LMP,266 days after date of ovulation for ART
• 23-24 weeks AOG
• Cardiac output increases, max by 30-50% at 20-24 weeks AOG
• Systemic vascular resistance decreases
• Increase in tidal volume and minute ventilation; decrease in
total lung capacity and reserve volumes
• Physiologic dyspnea
• Morning sickness (pathologic: hyperemesis gravidarum)
• Prolonged gastric emptying
• Decreased LES tone
• Ureteral dilatation
• Increased GFR by 50%
• Increased RAASactivation
• Increase in all clotting factors (fibrinogen and factors VII-X)
• Decreased fibrinogen turnover time
• Hyperestrogenic, euthyroid state
• Diabetogenic state - secondary to human placental lactogen
production
• Secondary to estrogen - spider angiomata, palmar erythema
• Secondary to melanocyte-stimulating hormone - linea nigra,
melasma, hyperpigmentation of nipples
• Increased by 300 kcal/day
• Weight gain: overweight - 15-25 lb, underweight - 28-40 lb
• Hct, blood type, RPR/VDRL, Rubella antibody,
Hepatitis B surface antigen, varicella titers, gonorrhea/
chlamydia, urine culture, early screening for aneuploidy,
preeclampsia screening
• Triple or quad screen, obstetric ultrasound, amniocentesis if
interested
• Hct, RPR/VDRL, glucose loading test (24-28 weeks via OGTT),
GBS culture
• Fetal tone, activity, breathing movement, amniotic fluid volume,
non-stress test
• L/S ratio > 2
531
I
.
EARLY PREGNANCY COMPLICATIONS
Most common site of implantation • Ampulla (70%), isthmus (12%), fimbriae (11%)

Classic triad of ectopic pregnancy • Vaginal bleeding, amenorrhea, missed menses

Strongest risk factor for ectopic

• Prior ectopic pregnancy
pregnancy
Classic laboratory finding for ectopic
• P-hCGlow for gestational age
pregnancy
Procedure for unstable ectopic
• Exploratory laparoscopy
pregnancy patients
Highest success for methotrexate
• Size <5 cm, serum p-hCG <5,000, no fetal heartbeat
therapy
Most common etiology for first
• Abnormal chromosomes
trimester spontaneous abortions
• Both have open cervices (eyes (l's) wide open),
with(-) bag of waters.
• Inevitable: compatible uterus, may or may not
Inevitable vs incomplete abortion
have FHTs
• Incomplete: incompatible uterus, no appreciable
FHTs, with passage of meaty material
• All three have closed cervices
• Threatened: (+) bleeding, compatible uterus, (+)
BOW,(+) FHTs - essentially pregnancy intact but
in danger of progression to complete abortion
Threatened vs missed vs complete
• Missed: incompatible uterus,(+) BOW,(-) FHTs-
abortion
essentially death of the fetus but other products of
conception are intact
• Complete: incompatible uterus,(-) BOW,(·) FHTs -
essentially back to pre-pregnancy state
• Dilatation and curettage for first trimester
Surgical management for abortions
• Dilatation and evacuation for second trimester
Most common cause of cervical
• Iatrogenic or traumatic
incompetence

• 20% after 1 spontaneous abortion

Risks of recurrent abortions • 25-30% after 2 spontaneous abortions
• 30-35% after 3 spontaneous abortions
Most common cause of abortion
• Hemorrhage and infection
mortality
Synthetic progesterone receptor
• RU-486 (mifepristone)
antagonist used for termination of
(not approved by the FDA,locally)
pregnancies
This chemotherapeutic agent and
dihydrofolate reductase inhibitor
• Methotrexate
is used off-label for termination of
pregnancy
The success of medical abortion is
• Misoprostol
improved when combined with a
(not approved by the FDA,locally)
prostaglandin analog, typically

532
PRENATAL SCREENING
Most common cause of
• Trisomy 21
Down syndrome

Screening components for • Triple screen (NT, PAPP-A, hCG)

Down syndrome • Quad screening (MSAFP,hCG, estriol, inhibin A)
• Blastocyst implantation week 1
• Trophoblast differentiation week 2
Early embryogenesis
• Gastrulation week 3
• Organogenesis week 3-8
Spina bifida ultrasound • Lemon sign (concave frontal bones)
signs • Banana sign (caudally pulled and flattened cerebellum)

NORMAL LABOR AND DELIVERY

• PROM - prelabor rupture of membranes
PROMvs PPROM
• PPROM- preterm (< 37 weeks AOG) PROM

• Pool test (positive if collection offluid in the vagina)

• Nitrazine test (positive if paper turns blue upon contact with secretion)
• Fern test (positive if with arborization of vaginal secretion under
microscope)
Tests for ROM
• Actim'" PROM (determination of placental alpha-
microglobulin-1)
• Tampon test (positive if tampon is dyed with indigo carmine after
dye is introduced to amniotic fluid via amniocentesis)

• CPEDS (consistency, position, effacement, dilatation, fetal

Components of the Bishop
station)
score
• s4 unfavorable for induction, ;e9 favorable

• Anterior: junction of frontal and parietal bones, larger, diamond-

Anterior vs posterior shaped
fontanelle • Posterior: junction of parietal and occipital bones, smaller,
triangular-shaped
• Early (head compression)
Etiologies of
• Late (uteroplacental insufficiency)
decelerations
• Variable (umbilical cord compression)

• EDFir ExtER Exp

Cardinal movements of
• Engagement, descent, flexion, internal rotation, extension,
labor
external rotation/restitution, expulsion

Limits for first stage labor • 20 hrs nulliparous, 12 hrs multiparous

Limitsfor second stage labor • 3 hrs nulliparous, 2 hrs multiparous

Three signs of placental

• Cord lengthening, gush of blood, uterine fundal rebound
separation
Median vs mediolateral • Mediolateral: most common, more painful, more wound
episiotomy infections, less frequently used, less extensions

• FORCEPS
Criteria for forceps
• Fully dilated, Operator experienced, Ruptured membranes,
delivery
CPD absent, Empty bladder, Position definite, Station at least+ 2

Most common indication

• Failure of labor progression
for CSdelivery
Greatest risk during
• Rupture of prior uterine scar
vaginal birth after CS

533
I
.
ANTEPARTUM HEMORRHAGE
Vasa previa
Most frequent indication for
peripartum hysterectomy
Circumvallate vs velamentous vs
succenturiate placenta
Classical sign of placenta previa
Risk factors for placenta previa
Test to determine extent of
fetomaternal blood transfusion
Primary cause ofabruptio placenta
Classical sign of abruptio placenta
Diagnostic sign of abruptio placenta
Most common cause of DIC in obstetrics
Risk factors for uterine rupture
Primary maternal complication of
uterine rupture
Diagnosis ofvasa previa rupture at the
time of vaginal bleeding
534
• Occurs when a velamentous cord insertion
causes the fetal vessels to pass over the
internal cervical os
• Uterine atony
• Circumvallate - membranes double back
over the edge of the placenta
• Velamentous - vessels insert between
amnion and chorion away from placental
margin
• Succenturiate - extra placental lobe
implanted away from the rest of the
placenta
• Painless vaginal bleeding, with a sentinel
bleed usually after 28 weeks AOG
• Prior cesarean section and uterine surgery
• Multiparity
• Multiple gestation
• Erythroblastosis
• Smoking
• History of placenta previa
• Increasing maternal age
• Kleihauer-Betke test
• Unknown
• Couvelaire uterus
• Retroplacental clot with overlying placental
destruction on examination
• Abruptio placenta
• Prior uterine scar(s)
• Classical CS scar
• Labor induction
• Use of uterotonics
• Hemorrhagic shock
• Apt test (examination for nucleated fetal
RBCs)
COMPLICATIONS OF LABOR AND DELIVERY
Principal goal oftocolysis
Prior to pharmacologic
management, preterm
contractions can be decreased
by
First-line treatment for
eclampsia
Magnesium toxicity
Antidote for magnesium
toxicity
Black box warning for
terbutaline use >24-48 hrs
Percentage of patients with
ruptured membranes going
into labor
Conjugatemeasurements
External version is
performed
Relative contraindications
for trial of labor of breech
presentation
Non-vertex presentation
landmarks
Most common position of the
fetus at labor onset
Risk factors for shoulder
dystocia
Maneuvers for shoulder
dystocia
During delivery, suspicion of
macrosomia is increased if
you see
• Delay delivery by at least 48 hrs
• Hydration ➔ decreases ADH (almost similar to
oxytocin) ➔ decreases binding to oxytocin receptors
➔ reduced contractions
, Mgso.
• 6-10 mg/dL- decreased tendon reflexes
• >10 mg/dL- respiratory depression, cardiac arrest
• 10 mL of 10% calcium gluconate or calcium chloride
for cardioprotection
• Pulmonary edema, cardiac events
• 50% within 24 hrs, 75% within 48 hrs
• Obstetric conjugate= Diagonal conjugate - 1.5 to 2 cm
• Before 36-37 weeks AOG;if not successful, repeat at
39 weeks
• Nulliparity
• 1500 g < EFW < 3500 g
• Incomplete breech
• Face - mentum
• Shoulder - acromion
• Breech - sacrum
• Occiput transverse; persistence leading to arrest oflabor
is common with platypelloid pelvis
• Fetal macrosomia • Maternal obesity
• Diabetes • Postterm deliveries
• Previous dystocia • Prolongedstage 2 oflabor
• McRoberts maneuver - straightening of the sacrum
relative to the lumbar vertebrae, rotation of the
symphysis pubis toward the maternal head, and a
decrease in the angle of pelvic inclination
• Suprapubic pressure - oblique-angle pressure to
dislodge anterior shoulder
• Rubin maneuver - pressure on accessible shoulder
toward the anterior chest wall to decrease the
bisacromial diameter
• Wood corkscrew maneuver - pressure behind the
posterior shoulder to rotate the infant and dislodge the
anterior shoulder under the symphysis pubis
• "turtle sign" (incomplete delivery of head; chin tucked
against perineum)
535
I
.
FETAL COMPLICATIONS OF PREGNANCY
Limits for fetal growth • >90th percentile: LGA, <10th percentile:SGA

Doppler investigation to
• Umbilical artery diastolic flow decreases or reverses
differentiate IUGRfetuses
Most classical risk factor for
• GDM
fetal macrosomia
• Rh positive fetuses with sensitized mothers ➔ maternal
antibodies cross the placenta ➔ hemolysis ➔ fetal anemia
Pathogenesis of Rh
➔ increased extramedullary hematopoiesis ➔ fetal hydrops
alloimmunization
• Hemolysis also causes bilirubin toxicity ➔ fetal neurologic
manifestations

Standard RhoGAM dose • 0.3 mg of Rh lgG for every 15 mL of fetal RBCs

Antibody titers associated with

• ;,1:16 titers
hydrops
Doppler investigation to
• Fetal MCAmeasurement
determine fetal anemia

Best treatment for IUFD • Delivery to avoid DICdevelopment

Routine induction oflabor

is advised when pregnancy • 41 weeks AOG
reaches
• Separation before differentiation of trophoblast
(before Day 3) - Di-Di (twin peak sign on UTZ)
• Separation after trophoblast differentiation and before
Events in twinning
amnion formation (Day 3-8) - Mo-Di (T sign on UTZ)
• Separation after amnion formation -
(Day 8-13) Mo-Mo or (Day 13-15) conjoined twins
• Vertex/vertex - trial of labor
• Vertex/non-vertex - trial of labor if twins are concordant
Delivery of twins
or presenting twin is larger
• Non-vertex/non-vertex - CS

HYPERTENSION AND PREGNANCY

Gestational • SBP ;,140 mm Hg and/or DBP ;,90 mmHg after 20 weeks AOG
hypertension • Deliver by 37 weeks
• SBP ;,140 mmHg and/or DBP ;,90 mmHg after 20 weeks AOG+
Preeclampsia without
proteinuria
severe features
• Deliver by 37 weeks
• Any of the following in a preeclampsia patient:
• SBP ;,160 mmHg and/or DBP ;,110 mm Hg
• Thrombocytopenia
Preeclampsia with • Renal insufficiency
severe features • Elevated liver enzymes
• Pulmonary edema
• Cerebral or visual symptoms
• Deliver by 34 weeks
• SBP ;,140 mmHg and/or DBP ;,90 mmHg before 20 weeks AOG
Chronic hypertension continuing up to at least 12 weeks postpartum
• Deliver by 38 weeks
• Hypertension before 20 weeks AOGwho develop proteinuria afterwards
Chronic hypertension
• Proteinuria before 20 weeks AOGwho develop sudden exacerbation
with superimposed
of HTN or proteinuria, along with other severe features
preeclampsia
• Deliver by 37 weeks; if with severe features, deliver by 34 weeks

536
 Primarily disease related
• Chronic hypertension
• Chronic renal disease
• Antiphospholipid antibody syndrome (APAS)
• Collagen vascular disease (e.g., SLE)
• Pregestational diabetes
• African-American
• Maternal age (<20 or >35)
Risk factors for preeclampsia
Primarily immunogenic related
• Nulliparity

.
• Previous preeclampsia
Multiple gestation
• Abnormal placentation
• New paternity, co-habitation <1 y

Family history
• Female relatives of parturient
One of the most interesting protective
• Smoking
factors against preeclampsia

Racial predilection for preeclampsia • African-Americans

Primary goal of antihypertensive therapy

• Stroke prevention
in preeclampsia
Primary goal of antihypertensive therapy
• Recurrent seizure prevention
in eclampsia
Most postpartum seizures in eclamptic
• First 48 hrs after delivery
patients occur within
Initiation of low-dose aspirin for
superimposed preeclampsia prevention • After 12 weeks AOG
should be started at
• Delivery; if eclamptic, stabilize first prior to
Definitive treatment for preeclampsia
delivery
Recurrence rate for those with preeclampsia
• 25-33%; if with chronic hypertension, 70%
in the first pregnancy
Drug of choice for antihypertensive
• Methyldopa, labetalol
maintenance

Drug of choice for acute lowering of BP • Hydralazine, labetalol

Therapeutic dose of MgSO4 • 4.8-8.4 mg/dL

537
I
.
DIABETES DURING PREGNANCY
Anti-insulin hormones during
pregnancy
Racial predilection for diabetes in
pregnancy
Screening for low-risk
populations
Screening for high-risk
populations
Initial treatment for GDMpatients
ADA diet plan calorie requirement
for GDMpatients
Glucose monitoring
Second-line treatment for GDM
patients
Commonly used insulin agents
Fetal monitoring for GDMpatients
Timing of delivery
Recurrence ofGDM
INFECTIOUS DISEASES IN PREGNANCY
Most common etiologic agent for
UTI
Major effects of asymptomatic
bacteriuria
Gold standard for diagnosing UTI
Acute cystitis vs pyelonephritis
Initial treatment for ASB
Most common complication of
lowerUTI
Management for pyelonephritis
Preferred medication for
influenza in pregnancy
Amsel criteria for bacterial
vaginosis
• Human placental lactogen/human chorionic
somatomammotropin
• Hispanics, Asian/Pacific Islanders, Native Americans
• Between 24-28 weeks AOG
• At first prenatal visit, then if negative, retest between
24-28 weeks AOG
• Lifestyle modification
• 2,200 calories per day, 200-220 g of carbohydrates per
day
• Fasting + three postprandial values
• Insulin or oral hypoglycemic agents if uncontrolled by
diet and with >25-30% elevations
• Short-acting: Humalog, NovoLog
• Intermediate-acting: NPH
• BPP between 32-36 weeks and done weekly /biweekly
• EFW estimation between 34-37 weeks AOG
• Induction of labor at 38 weeks AOG
• If EFW 2:4,000 g - elective CS delivery at 39 weeks AOG
• >50%, with 25-35% developing overt diabetes within
5 years
•E.coli
• Preterm birth, low birth weight
• Positive urine culture 2:100,000 CFU/mL
• Acute cystitis - lower urinary tract symptoms and
suprapubic discomfort
• Pyelonephritis - fever,Hankpain,+ acute cystitis symptoms
• Amoxicillin, nitrofurantoin, TMP-SMX,cephalexin
• Pyelonephritis
• Hospital admission, hydration, IV antibiotics
• Oseltamivir
. Presence of thin, white or gray, homogeneous
discharge coating the vaginal walls
• An amine (or "fishy") odor noted with addition of 10%
KOH("whiff" test)
• pH of greater than 4.5
• Presence of more than 20% of the epithelial cells as
"clue cells"
538
GBS culture is done during
Risk based criteria for GBS
treatment for women with
unknown GBSstatus
Diagnosis of chorioamnionitis
(Triple I)
Common etiologic agent for
chorioamnionitis
Congenital HSV infection
Congenital varicella syndrome
Post-exposure prophylaxis for
varicella
Congenital CMVinfection
Congenital rubella syndrome
Cornerstone drug for babies born
to HIV-infected women
Neonatal infection of
N. gonorrhoeae
Neonatal infection of
C. trachomatis
Gold standard for gonorrhea/
chlamydial diagnosis
Prophylaxis for neonates born to
HBV-positive mothers
Late congenital syphilis
Screening for syphilis
Confirmatory tests for syphilis
Only known hosts for
Toxoplasma gondii
Recommended treatment for
pregnant women
Congenital Zika infection is
notably associated with
• 35-37 weeks AOG
• Labor before 37 weeks of gestation
• ROMgreater than 18 hours
• Temperature >100.4°F
• Fever 2:39°Cor 102.2°F based on oral maternal
temperature with another clinical sign, including
0 elevated maternal WBC count (>15,000/mL)
0 purulent fluid from cervical os
0 fetal tachycardia (>160 beats per minute), or
0 microbial evidence from an amniocentesis
• Polymicrobial
• Chorioretinitis, microcephaly, hydrocephalus
• Skin scarring, limb hypoplasia, chorioretinitis,
microcephaly
• VZIGup to 10 days after exposure
• Oral acyclovir (800 mg, Sx/day x 7 days) or
oral valacyclovir (1,000 mg, 3x/day x 7 days)
• Most common cause of congenital viral infection
• Most common cause of congenital hearing loss
• Blueberry muffin baby (jaundice + thrombocytopenic
purpura)
• "Bobo, bu log, bingi, butas ang puso"
• CNSdefects, cataracts/retinopathy, deafness, cardiac
defects (most common is PDA,but supravalvular
pulmonic stenosis is most pathognomonic)
• Zidovudine
• Ophthalmia neonatorum, necessitating universal
erythromycin ointment as prophylaxis
• Neonatal conjunctivitis and/or Chlamydia pneumonia
• NAAT(culture is previous gold standard)
• HBlg within 12 hrs after birth and hepatitis B
vaccination series
• Saber shins, mulberry molars, Hutchinson teeth, saddle
nose, neurologic manifestations
• VDRL,RPR (false positives: SLE,APAS)
• FTA-ABS,TPPA
• Wild and domestic cats
• Maternal infection - spiramycin, fetal infection -
pyrimethamine and sulfadiazine + folic acid
• Microcephaly
539
I
.
OTHER MEDICAL COMPLICATIONS OF PREGNANCY
Hyperemesis gravidarum (HG)
symptoms
First-line antiemetics for HG
Best predictor of seizure
frequency
Increased seizure frequency in
pregnant women is due to
Most common congenital
abnormalities in infants born to
epileptic mothers
Lowest neurodevelopmental
outcomes in epileptic mothers
maintained on
Mechanisms of teratogenicity
Changes in anti-epileptic
drug (AED) administration in
pregnancy
Prevention of increased risk of
hemorrhage in newborns from
epileptic mothers maintained on
AEDs
Surgical repair of cardiac lesions
must be done
Most common right-to-left shunts
among pregnant mothers
For women with moderate to
severe valvular disease, the ideal
management would be
Management for pregnant women
with Marfan syndrome
Criteria for peripartum
cardiomyopathy diagnosis
Virchow triad
Classical sign of superficial vein
thrombosis
Majority of deep vein thrombosis
(DVT) patients will have
unilateral symptoms at the
Diagnostics for DVT
Treatment for DVT
Warfarin embryopathy
• Persistent vomiting, weight loss >5% of prepregnancy
weight, ketonuria
• Promethazine
• Number of seizure episodes in prepregnancy year
• Increased P450 function
• Increased volume of distribution (Vd)
• Hypervolemia
• Sleep deprivation and stress
• Cleft lip and palate (4x), cardiac anomalies (3x)
• Lamotrigine
• Folate deficiency
• Epoxide generation
• Switch to single AED
• 3x-4x/day dosing instead of standard 2x/day dosing
• Folate supplementation
• Monthly serum AEDlevels
• Aggressive vitamin K supplementation towards the end
of pregnancy
• At least a year before pregnancy
• PDA,VSD
• Surgical treatment prior to becoming pregnant (but
pulmonary stenosis can be managed with valvuloplasty
during the pregnancy)
• Sedentary lifestyle and beta blockers
• Heart failure symptoms during pregnancy
• Dilated heart with EF at 20-40%
• Hypercoagulability
• Endothelial damage
• Venous stasis
• Palpable, usually visible, venous cord that is tender,
erythematous, and edematous
• Left leg (90%)
• Initial test - Doppler ultrasound
• Gold standard - venography
• LMWH(enoxaparin)- preferred
• Unfractionated heparin (IV heparin) - transitioned to
subcutaneous heparin afterwards
• Nasal hypoplasia, skeletal abnormalities, optic atrophy
540
Symptoms of pulmonary em bolus • Acute dyspnea with pleuritic chest pain, hemoptysis/
(PE) tachycardia, and/or concomitant signs of DVT
Gold standard for PE diagnosis • Pulmonary angiography
• LMWH (enoxaparin) - first choice
• Unfractionated heparin (IV heparin) - ifhypotensive
Treatment for PE
or unstable
• Streptokinase - if massive PE
Most common cause of
• Graves disease
hyperthyroidism in pregnancy
Most common cause of
• Hashimoto thyroiditis
hypothyroidism in pregnancy
Systemic lupus erythematosus
• 1/3 resolves, 1/3 progresses, 1/3 unchanged
(SLE) prognosis in pregnancy
Two distinct manifestations of • Lupus syndrome
neonatal lupus • Irreversible congenital heart block
Most commonly abused
• Alcohol and cigarette
substances in pregnancy
Most commonly abused illicit drug
• Marijuana
in pregnancy
• Growth retardation
Fetal alcohol syndrome • Abnormal facies
• CNSeffects (mental retardation)
Primary treatment for smoking • Smoking cessation programs
Most common narcotics used in
• Oxycodone, heroin, methadone
pregnancy

POSTPARTUM CARE AND COMPLICATIONS

Letdown usually begins by • 24-72 hrs postpartum

Rh negative patients should

receive RhoGAM IM injection • 72 hrs postpartum
within
Best contraception during the • Tubal ligation [intrauterine device if with no consent
postpartum period for ligation)
Most common implantable
progestin offered during the • Etonogestrel implant (e.g., Implanon NXT")
postpartum period
If using oral combined
contraceptive pills postpartum, • At least 4 weeks postpartum if not breastfeeding
the patient must wait
Nonhormonal contraceptives
that can be used in the immediate • Copper IUD,condoms
postpartum period

541
I
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Postpartum fever differentials
Hematoma is suspected if
Management for retroperitoneal
hematoma
Leading cause of postpartum
hemorrhage
Management of uterine a tony
Effective method to reduce blood
loss associated with uterine atony
if without IV access
Surgical management of blood loss
associated with uterine atony
Management for retained
products of conception
Risk factors for placenta accreta
Risk factors for uterine rupture
Management of uterine rupture
Risk factors for uterine inversion
Management of uterine inversion
Risk factors for endometritis
Diagnosis of cellulitis
Diagnosis of abscess
Diagnosis ofnecrotizing fasciitis
Wound separation vs wound
dehiscence
Drug of choice for mas ti tis
Diagnosis of breast abscess
Drug of choice that may be used
for postpartum blues
• Atelectasis (wind) • Day0
• UTl (water] • Day 1-2
• Endometritis (womb) • Day 2-3
• Wound infection (wound) • Day 4-5
• Septic pelvic thrombophlebitis (walk) • Day 5-6
• Mastitis • Day 7-21
• There is a larger than expected drop in hematocrit
• Embolization
• Uterine atony
• IV oxytocin + uterine massage ➔
methylergonovine (contraindicated in asthma) ➔
PGF2a (contraindicated in asthma)
• IMpreparations (oxytocin, carboprost,
methylergonovine)
• Rectal or sublingual misoprostol (not approved by the
FDAlocally)
• Bakri balloon, uterine artery embolization ➔
exploratory laparotomy (internal iliac artery ligation,
compression sutures, hysterectomy)
• Uterine exploration ➔ dilatation and curettage
• Placenta previa, prior uterine surgery
• Previous uterine surgery, breech extraction, obstructed
labor, high parity
• Exploratory laparotomy ➔ repair of rupture ➔
hysterectomy
• Fundal implantation of the placenta, uterine a tony,
placenta accreta, excessive traction during third stage
• Manual replacement+/· uterine relaxants ➔
exploratory laparotomy (Huntington, O'Sullivan)
• Meconium, chorioamnionitis, prolonged ROM
• Local erythema around surgical site, expanding after
12-24 hrs
• Cellulitis nonresponsive to medications, with increasing
fever or palpable collection of pus
• Loss of pain from the cellulitis site due to nerve damage
• Separation of skin only vs separation of fascia
• Dicloxacillin
• Mastitis nonresponsive to medications
• SSR!s
542
 SECTION
BENIGN DISORDERS OF THE LOWER GENITAL TRACT
Most common etiology of
congenital labial fusion
Most common etiology
ofprepubertaland
postmenopausal labial fusion
Laboratory findings in
congenital adrenal hyperplasia
(CAH)
Treatment for CAH
Outflow tract obstructions
Etiology of imperforate hymen
Etiology of transverse vaginal
septum
Etiology of vaginal atresia
Vaginal atresia vs Mullerian
agenesis (MRKH syndrome)
Lichen sclerosus vs lichen
plans vs lichen simplex
chronicus
Treatment of lichen diseases
Most common vulvar tumor
Management for hidradenitis
suppuritiva
Management of Bartholin duct
cysts
DES exposure results to a
rare form of carcinoma of the
cervix and vagina, which is
Mucus-filled retention cysts of
the cervix
TWO
GYNECOLOGY
• Excess androgens
• Hypoestrogenism
• Elevated 17-alpha-hydroxyprogesterone or urine
17-ketosteroid with decreased serum cortisol
• Exogenous cortisol; if with salt wastage, give also
mineralocorticoid
• lmperforate hymen,transverse vaginalseptum, vaginalatresia
• Nondegeneration of central portion of the junction
between the urogenital sinus and sinovaginal bulbs
• Noncanalization of Mullerian tubercle, leaving a septum
behind
• Noncontribution of the urogenital sinus to the lower vagina
• Developed Mullerian system vs absent Mullerian system
• LS (white thinned skin)
• LP (Wickham's striae)
• LSC (thickening of the skin)
• Medium to high potency topical steroids
• Epidermal inclusion cysts
• Antimicrobial skin wash and ointments; if with
abscess, excision or incision and drainage
• If small and asymptomatic, sitz baths
• If abscess, Word catheter or marsupialization
• If occurring in women >40 years old, biopsy should
be performed
• Clear cell adenocarcinoma
• Nabothian cysts
543
I
'
BENIGN DISORDERS OF THE UPPER GENITAL TRACT
Notable association ofuterine septums
Notable associations ~fbicornuate or
unicornuate uterus
Modality to distinguish bicornuate and
septate uterus
Treatment for septate uterus
Most common systemic abnormality
associated with uterine abnormalities
Most common type of uterine leiomyoma
Most common type of uterine leiomyoma
associated with bleeding
Distinguishing feature between
leiomyoma and adenomyosis
Racial predilection for leiomyoma
Most common symptom ofleiomyomas
Difference in bimanual examination
findings in leiomyoma vs adenomyosis
One of the newest modalities for
leiomyoma treatment
Definitive management for leiomyomas
Associated risk with power morcellation
in minimally invasive myomectomy
In postmenopausal women, endometrial
polyps must be removed since
Theories on the pathogenesis of
endometriosis
Hallmark sign of endometriosis
Definitive diagnosis of endometriosis
Best management option for endometriosis
Medical management of endometriosis
Definitive management for
endometriosis
Theories on the pathogenesis of
adenomyosis
Most common sign of adenomyosis
Diagnostics for adenomyosis
Most effective temporizing treatment
adenomyosis prior to hysterectomy
• First-trimester spontaneous abortion
• Preterm labor
• MRI or laparoscopy
• Operative hysteroscopy
• Renal anomalies
• Intramural
• Submucosal
• Presence of a pseudocapsule
• African American
• Abnormal uterine bleeding
• Lumpy-bumpy or cobblestone protrusions vs
smooth, boggy
• Magnetic resonance-guided focused ultrasound
surgery
• Hysterectomy
• Spreading an undiagnosed uterine sarcoma
• Bleeding from endometrial polyps may mask
bleeding from another source, such as an
endometrial intraepithelial neoplasia (EIN) or
carcinoma
• Ectopicendometriumtravelsvia lymphatics(Halban)
• Metaplastic transformation (Meyer)
• Retrograde menstruation (Sampson)
• Cyclic pelvic pain before menses
• Direct visualization
• Surgical management
• Induction of pseudopregnancy ➔ induction of
pseudomenopause
• Total hysterectomy and bilateral salphingo-
oophorectomy
• Direct endometrial invasion through the
myometrium
• Metaplastic transformation of Mullerian rest cells
• Prolonged or heavy menstrual bleed
• MRI (most accurate)
• Pelvic ultrasound (most common)
for
• Levonorgestrel-containing IUD
544
Definitive managem_enf for adenomyosis
Most common functional ovarian cysts
Ovarian cysts resulting from elevated
13-hCG
Endometriomas are also called
Indications for surgical management in
ovarian cysts
INFECTIONS OF THE LOWER FEMALE REPRODUCTIVE TRACT
Most common cause ofvulvitis
Characteristic lesions of Crohn disease
Phases of syphilis infection
Drug of choice for syphilis
Acute febrile reaction after therapy for
syphilis
Characteristic lesions of HSV infection
Diagnostics for HSV infection
Treatment for HSV infections
Characteristic lesion of chancroid
Diagnostics for H. ducreyi
Treatment of chancroids
C. trachomatis serotypes that cause
lymhpgranuloma venereum (LGV)
Phases of LGVinfection
Treatment of LGVinfection
Most clinically evident result of HPV
infection
Most common HPV causing genital warts
Medicaltreatment for condyloma acuminata
Characteristic lesion of molluscum
contagiosum
Treatment of molluscum contagiosum
Pediculosis vs scabies
Treatment of pediculosis
• Hysterectomy
• Follicular cysts
• Theca lutein cysts
• Chocolate cysts, from thick brown old blood
collected inside
• Acutely symptomatic with pain, hemorrhage, or
infection
• Growth observed
• Candidiasis
• Linear; knife-cut ulcers
• Primary syphilis - painless chancre
• Secondary syphilis - fever,myalgias,
maculopapular rash on palms or soles
• Tertiary syphilis - gummas, aortitis, tabes dorsalis
• Penicillin
• Jarisch-Herxheimer reaction
• Multiple vesicles evolving into painful genital
ulcers
• NAAT(primary method), Tzanck smear
(historical)
• Acyclovir;famciclovir;or valacyclovir
• Painful, nonindurated ulcer ("beefy red")
• Gram stain ("school of fish"). but mainly a
diagnosis of exclusion
• Ceftriaxone, azithromycin, ciprofloxacin, or
erythromycin
• Ll, L2, L3
• Primary - painless pa pule or shallow ulcer
• Secondary - inguinal syndrome
• Tertiary - anogenital syndrome
• Doxycycline or erythromycin
• Condyloma acuminata
• HPV6, 11
• Trichloroacetic acid, podophyllin. 5-fluorouracil
• Small, domed papule with umbilicated center
("water wart'')
• Excision, trichloroacetic acid, or cryotherapy
• Phthirus pubis vs Sarcoptes scabiei, pubic hair vs
possible systemic spread
• Permethrin or pyrethrins with piperonyl
I
butoxide
545 '
Treatment of scabies
Gold standard for diagnosis of bacterial
vaginosis
Primary complaint in bacterial vaginosis
Treatment of bacterial vaginosis
Primary complaint in candidiasis
Treatment of candidiasis
Considered the most common ST!
Primary complaint in trichomoniasis
Diagnostics for trichomoniasis
Treatment oftrichomoniasis
Most common etiologies of
mucopurulent cervicitis
Diagnostics for N. gonorrhoeae
Treatment for gonorrhea
Diagnostics for C. trachomatis
Treatment for chlamydia
INFECTIONS OF THE UPPER FEMALE REPRODUCTIVE TRACT
Treatment regimens for
endomyometritis
Most common serious complication ofSTis
Most serious complication of PID
Principal symptom of PID
Fitz-Hugh-Curtis syndrome
Primary treatment for PID
Symptoms of tuba-ovarian abscess
(TOA)
Diagnostics for TOA
Toxin responsible for toxic shock
syndrome (TSS)
Highest priority in management ofTSS
Antibiotic treatment for TSS
Diagnostics for HIV
• Permethrin or ivermectin
• Gram stain and demonstration of bacterial
presence
• Malodorous discharge
• Metronidazole or clindamycin
• Pruritus (only 20% experience the white curd-
like discharge)
• Fluconazole
• Non-albicans: boric acid
• Trichomoniasis vs chlamydia
• Profuse frothy discharge (only 10% experience
the "strawberry cervix")
• Wet prep (most common), culture (gold standard)
• Metronidazole or tinidazole
• N. gonorrhoeae, C. trachomatis
• Intracellular gram-negative diplococcus ("paired
kidney beans")
• Thayer-Martin chocolate agar
• NAAT(gold standard)
• Ceftriaxone or cefixime AND azithromycin
• Intracellular, unicellular, non-gram staining
round bodies
• NAAT(gold standard)
• Azithromycin or doxycycline
• Clindamycin and gentamicin; add doxycycline if
chlamydia is suspected
• Pelvic inflammatory disease
• Infertility
• Abdominal/pelvic/adnexal pain
• Perihepatitis secondary to PID with "violin-
string adhesions"
• Cefoxitin or cefotetan AND doxycycline
• Adnexal or posterior cul-de-sac mass in the setting
of PID,with pain
• Ultrasound (study of choice)
• Laparoscopy (gold standard)
• TSST-1 from S. aureus
• Supportive treatment ofhypotension
• Clindamycin and vancomycin
• ELISA(screening), Western blot (confirmatory)
546
PELVIC ORGAN PROLAPSE (POP)
• Level 1 - cardinal and uterosacral ligaments
(compromise: apical prolapse)
De Lancey levels of vaginal support
• Level2 - levator ani (compromise: cystocele, rectocele)
• Level 3 - perinea! body (perinoecele, urethrocele)

• Advanced age and menopause

• Parity (especially, vaginal deliveries, obstructed
Risk factors for POP labor, traumatic delivery)
• Elevated intraabdominal pressure
• Hysterectomy
• Separating the labia, viewing the vagina, while
Pelvic relaxation is best observed by
patient coughs or performs Valsalva
Rectal relaxation is best observed by • Rectal examination
Used to visualize cystocele, rectocele,
• Split speculum examination
or enterocele
Complete uterine prolapse is also called • Procidentia uteri
• Baden-Walkey Halfway Scoring System
Scoring systems for POP
• Pelvic Organ Prolapse Quantitative (POP-Q)Scale
First-line therapy for mild symptoms • Kegelexercises,pelvic floor therapy with biofeedback
Mainstay of conservative management • Pessary
Surgical management for cystocele
• Anterior and posterior colporrhaphy
and rectocele correction
Surgical management for enterocele • Vaginal enterocele repair
Surgical management for significant
• Hysterectomy with apical suspension
uterine prolapse

URINARY INCONTINENCE
• Stress incontinence (involuntary urine
Most common type of incontinence
loss on physical exertion)
• Overflow incontinence (detrusor
More common type of incontinence in men
underactivity or bladder outlet obstruction)

Involuntary urine loss associated with urgency • Urgency incontinence

Incontinence secondary to a urinary fistula,

• Continuous incontinence
urethral diverticulum, or ectopic ureter
Incontinence often seen in elderly with limited
• Functional incontinence
mobility and those with dementia
Strong independent risk factor for urinary
• Type 2 diabetes mellitus
incontinence
Sympathetic control of the bladder • Hypogastric nerve (T10 - L2)
Parasympathetic control of the bladder • Pelvic nerve (S2 - S4)
Most common management option for stress
• Surgery
incontinence
Most common management option for urgency
• Anticholinergic drugs
incontinence
Management for overflow incontinence • Cholinergic drugs

Management for urinary fistulas • Surgery

547
I
.
PUBERTY, THE MENSTRUAL CYCLE, AND MENOPAUSE
Pubertal sequence
Average years after menarche for ovulation
regularization
Delayed menarche is common in these
populations
Precocious puberty
The ovarian follicle produces
The corpus luteum produces
Two-cell theory or two-cell, two-
gonadotropin theory
Resumption of meiosis in the oocyte is
triggered by
Fertilization must occur within this time
period before egg degenerates
Upon fertilization, the developing
trophoblast produces this hormone to
maintain corpus luteum function
Phase of endometrial cycle under estrogen
control
Phase of endometrial cycle under
progesterone control
Phase of endometrial cycle under
progesterone withdrawal
Perimenopause occurs
Hormonal changes during perimenopause
Definition of menopause
Average age of menopause
Most common cause of primary ovarian
insufficiency
Menopausal symptoms
Only indication for menopausal hormone
therapy (MHT) as TREATMENT
548
• Thelarche, pubarche, accelerated growth,
menarche
• 2years
• Athletic women, or women with lesser body
fat
• Pubarche or thelarche before 8 years old
• Estrogen
• Estrogen and progesterone (progesterone is
higher)
• LH stimulates production of androgens in
theca cells ➔ transport to granulosa cells,
where FSH stimulates androgen to estrogen
conversion
• LH surge
• Within 24 hrs
• Beta-hCG; until 8-10 weeks AOG
• Proliferative
• Secretory
• Menstrual
• 2-8 years prior to menopause
• Decreased follicle number ➔ reduced inhibin
8 secretion ➔ FSH rises and progesterone
levels are low
• 12 months of amenorrhea after the final
menstrual period
• 51 years old (range 48-52 years)
• 48 years old: Filipinos
• Idiopathic or autoimmune
FSH IUL (FSH >40 IU/L is diagnostic)
• Flushes, forgetfulness
• Sweats at night, sad (depression), stroke,
skeletal changes (osteoporosis)
• H eart disease
• Insomnia
• U rinary symptoms, urogenital atrophy
• Libido decreases
• Moderate to severe vasomotor symptoms
(VMS)or genitourinary syndrome of
menopause (GSM)
Only indication for MHT as PREVENTION • Osteoporosis

• Increased DVTs,PE, ischemic stroke, invasive

RisksofMHT
breast cancer
For women with intact uterus, unopposed
estrogen is contraindicated, and this • Progestin to prevent E!N, EH, and EM cancer
hormone is added
Only FDAapproved nonhormonal
• Paroxetine
medication for VMS
Treatment for vaginal and urogenital atrophy • Low-dose vaginal estrogen
SHATTERED Family
• S teroid use
• H yperthyroidism/hyperPTH/hyperCa
• A !coho! and tobacco use
• Thin
Risk factors for osteoporosis • T estosterone low
• E arly menopause
• Renal or liver failure
• E rosive bone disease
• Dietary Ca low, DM Type I
• Family history
Gold standard for osteoporosis diagnosis • DXA(T-score :52.S denotes osteoporosis]
Drug used for prevention and treatment
• Bisphosphonates
for osteoporosis

549
I
.
AMENORRHEA
Primary amenorrhea
Secondary amenorrhea
Breasts present, uterus absent
Breasts absent, uterus present
Most common enzyme defect in
congenital adrenal hyperplasia
(CAH)
Confirmatory test for CAH
Kallmann syndrome
Most common cause of secondary
amenorrhea
Asherman syndrome
Diagnostic criteria for polycystic
ovary syndrome (PCOS)
Progesterone challenge test
procedure
ABNORMALITIES OF THE MENSTRUAL CYCLE
Dysmenorrhea
Primary dysmenorrhea
Most common misdiagnosis of
primary dysmenorrhea
First-line medication for primary
dysmenorrhea
Management for cervical stenosis
Diagnosis of premenstrual syndrome
(PMS)/premenstrual dysphoric
disorder (PMDD)
First-line management for PMS/PMDD
Formertermforheavymenstrualbleeding
Former term for light menstrual bleeding
Formerterm for intermenstrual bleeding
• Absence of menarche by 15 years old
• Absence of secondary sexual characteristic development
by 13 years old
• Absence of menses for 3 months if with regular cycles
• Absence of menses for 6 months if with irregular cycles
• Mullerian agenesis or testicular feminization
• Hypergonadotropic hypogonadism
• Defects in steroid pathways
• Hypogonadotropic hypogonadism
• 21-alpha-hydroxylase
• (Others: 11-beta-hydroxylase, 3-beta-hydroxysteroid
dehydrogenase)
• ACTHstimulation test
• Hypogonadotropic hypogonadism and anosmia
• Pregnancy
• Intrauterine adhesions
Rotterdam criteria (2/3)
• Oligo/anovulation
• Hyperandrogenism
• Polycystic ovaries
• Oral progesterone for 7-10 days
• If(-) withdrawal bleeding ➔ estrogen and progesterone
challenge
• If still(-) withdrawal bleeding ➔ outflow tract disorder.
• If (+)withdrawal bleed after estrogen and progesterone
challenge ➔ hypothalamic-pituitary disorder vs ovarian
failure
• Pain during menstruation that interferes with
normal activities
• Associated with ovulatory cyclesand absence of organic
cause
• Endometriosis
• Prescription-strength NSA!Ds
• Dilation of cervix via mechanical dilators or laminaria
• Symptoms must occur 2 weeks prior to menstruation
• Symptoms must resolve after onset of menses
• At least 7-day symptom free interval in the first half
of the menstrual cycle
• Symptoms must occur in at least two consecutive cycles
• SSRls
• Menorrhagia (excessive days or volume flow)
• Hypomenorrhea (regularly timed, light flow)
• Metrorrhagia (any bleeding between normal menses)
550
 • Menometrorrhagia (excessive bleeding at irregular
Formerterm for heavy irregular bleeding
intervals)
Former term for infrequent
• Oligomenorrhea (irregular cycles> 35 days apart)
menstrual cycles
Etiologies of abnormal uterine • Structural: PALM
bleeding (AUB) • Non-structural: COEIN
Best treatment of acute hemorrhage
• IV conjugated estrogen
fromAUB
Most common cause of
• Endometrial and/or vaginal atrophy
postmenopausal bleeding
Expected EMstripe thickness for
• s4mm
postmenopausal women

CONTRACEPTION AND STERILIZATION*

• Effectiveness: 55-80%
Periodic abstinence
• Primary disadvantage: unreliable
• Effectiveness: 27%
Coitus interruptus
• Primary disadvantage: high failure rate
• Effectiveness: 45-85%
Lactational amenorrhea
• Primary disadvantage: unreliable
Conditions for successful • Breastfeeding should be only form of infant nutrition
contraception with lactation • Used only as long as woman has amenorrhea
amenorrhea • Used only for a maximum of six months
• Effectiveness: 85-90%
Male condoms • Primary advantage: protection against STI
• Prima1y disadvantage: Hypersensitivity, coital interruption
How to maximize male condoms • Leave a well at the tip
• Effectiveness: 80-85%
Female condoms • Primary advantage: protection against ST!
• Primary disadvantage: cost and bulkiness
• Effectiveness: 80-85%
Vaginal diaphragm
• Possible complications: TSS, UTI
• Effectiveness: 68-84%
Cervical cap
• Most common cause of failure: dis lodgment
• Effectiveness: 70-75%
Spermicide
• Most common compound: nonoxynol-9, octoxynol-9
Most commonly used reversible
• IUD
contraception
• Copper containing IUD [Paragard) - also used for
Two forms of IUD emergency contraception
• LNGcontaining IUD (Mirena) - also used for AUB
• Para Gard - 0.8% (first year), 1.9% (10-year)
Failure rates for IUDs
• Mirena - 0.2% (first year), 0.7% (5-year)
- • Effectiveness: 92%
Combination oral contraceptive
• Most common cause of discontinuation: nausea, -
pills (OCPs)
breakthrough bleed, daily intake
Only antibiotic that reduces COC
• Rifampin
effectiveness

551
I
..
 • Suppression of LH
Contraceptive effects of
• Induces a thin, decidualized EM unreceptive to implantation
progestins
• Thickens sperm mucus
Contraceptive effects of
• Suppression of FSH
estrogens
Low-dose COCcontain • ,;35 mcg of ethinyl estradiol (EE]
High-dose COCcontain • 50 mcg of EE
Complications associated with • Thrombotic events, stroke, MI, benign hepatic tumors,
coc gallbladder disease
Transdermal contraceptive
• Higher by 60% estrogen exposure
patch
Vaginal ring • Lower hormone exposure
• Effectiveness: 92%
Progestin-only contraceptive
• Taken every day of the cycle at the same time
pills {POPs)
(3 hrs delay= missed pill)
• Does not interfere with breastfeeding
Advantages of POPs
• Given for those with contraindications to estrogen
• Effectiveness: 97%
Injectable progestin
• Given every 3 months
{Depo-Provera)
• Most common cause of discontinuation: irregular bleeding

• Effectiveness: 99.5%
Implantable progestin • Provides 3 years of uninterrupted protection
{Nexplanon) • Most highly effective reversible contraception
• Most common cause of discontinuation: irregular bleeding
• Morning-after pill
Emergency contraception
• ParaGard
options
• Ulipristal acetate
• 1.5 mg LNGsingle dose OR
Plan B for emergency
• 0.75 mg LNGq12 for two doses
contraception
• Taken within 72 hrs of intercourse
ParaGard for emergency
• Inserted within 120 hrs of intercourse
contraception
Ulipristal acetate for emergency
• 30 mg single dose within 120 hrs after intercourse
contraception
Most common technique of tubal
• Modified Pomeroy technique
sterilization
Window period until vasectomy
• 3 months and/or 20 ejaculations
becomes fully effective

'Effectiveness ranges for cited contraceptive techniques are obtained from Blueprints Obstetrics and
Gynecology, 7th edition.

552
INFERTILITY
• Failure of a couple to conceive after 12 months of
Infertility
unprotected intercourse
Fecund~bility • Ability to achieve pregnancy in one menstrual cycle
• 20% - within 1 month
Average conception rates for • 60% - within 6 months
couples • 75% - within 9 months
• 80% - within 12 months
• 10% - unexplained
-
Contribution of factors to • 10-20% - combination of male and female factors
infertility • 35% - male factor only
• 45-55% - female factor only
Most common cause of oligo/
• PCOS
anovulation
Most common cause of tubal
• PID
infertility
Most common aneuploidy
• 45XO (Turner syndrome)
associated with female infertility
• Clomiphene citrate on Day 5-9, and measurement of FSH
on Day 3 and 10
• Day 3 FSH (<10 mlU/mL is adequate, >20 mIU/mL is poor)
• Day 3 estradiol (<80 pg/mL is adequate, >80 pg/mL is poor)
Assessment of ovarian reserve
• Day 2-4 antral follicle count (4-10 antral follicles is
~, adequate, <4 is poor)
• AMHmeasurements (>0.5 ng/mL is adequate, <0.15 ng/mL
is poor) ~

• Clomiphene citrate - antiestrogen

• Human menopausal gonadotropin - FSH/LH analog
• Recombinant GnRH - stimulates FSH/LH release
Ovulation induction
• Letrozole - aromatase inhibitor
• Bromocriptine: for hyperPRL
• Metform - biguanide

Major side effects of ovulation

• Multiple gestation, ovarian hyperstimulation
induction
Most common reversible cause
• Varicocele
of male factor infertility
• Volume 2:1.5 mL
• pH >7.2
• Concentration> 15 million/mL
Normal seminalysis parameters
• Sperm count >39 million per ejaculate
• Morphology 2:4% normal forms
• Motility >32% with forward progression
• Gamete intrafallopian transfer (GIFT): if with functional
fallopian tubes, oocytes and sperm are placed into the FT
laparoscopically
In vitro fertilization
• Zygote intrafallopian transfer (ZIFT): in vitro fertilization
modifications (from Lentz)
for 24 hrs, then transferred
• Tubal embryo stage transfer (TEST): in vitro fertilization
for 8-72 hrs, then transferred

Only antibiotic that reduces COC

• Rifampicin
effectiveness

553
I
'
VULVAR AND VAGINAL NEOPLASIA
Risk factors for VIN
Characteristic iesions of extramammary
Paget disease of the vulva
Most common type of vulvar cancer
Most common location ofvulvar cancer
Most common surgical staging approach
for vulvar cancer
Treatment for vulvar cancer
Prognostic factor for melanoma of the
vulva
Most common type of vaginal cancer
Most common type of vaginal cancer
associated with DES exposure
Treatment for vaginal cancer
CERVICAL NEOPLASIA
Top cancer killer of women in the
developing world
Highest oncogenic potential among
HPVserotypes
Types ofHPVvaccines
Risk factors for cervical cancer
Initiation of cervical cancer
screening
Screening frequency and modalities
• HPV 16 and 18 infection, cigarette smoking,
immunodeficiency
• Longstanding pruritus with beefy red lesions,
eventually becoming eczematous white plaques
• Squamous cell carcinoma
• Labia majora
• Radical vulvectomy with inguino-femoral lymph
node dissection
• Stage I - radical local excision
• Stage II - radical local excision with lymph node
dissection or radical vulvectomy
• III - radical vulvectomy or chemoradiation
• IV- chemoradiation ± radiotherapy
• Depth of invasion
• Squamouscell carcinoma
• Clear cell adenocarcinoma
• Stage I - surgical management
• All others - chemoradiation
• Cervicalcancer
• HPV 16, 18
• Cervarix (16, 18)
• Gardasil (6, 11, 16, 18)
• Gardasil-9 (6, 11, 16, 18, 31, 33, 45, 52, 58)
• Persistent high risk HPV type ( necessary cause of
cervical cancer)
• Parity of 7 or more
• OCP use >5 years with HPV
• Current smokers & younger age at smoking
• Co-infected with Chlamydia or HSV-2
• HIV
• Early age at sex <14 years old
• Sex partners >6
• Pregnancy <17 years old
• No cervical cancer screening
• Low socio-economic status
• Poor access to healthcare services, poor nutrition, etc.
• Age 25
• 25-65 years old: Pap smear every three years, co-
testing every five years,
primary HPV typing every five years, or
visual inspection with acetic acid (VIA) every five
years in low-resource settings
554

Cessation of screening
Screening after total hysterectomy
Screening after history of CIN 11/111
Management of ASC-US
Management of ASC-H
Management of LSIL
Management of HSIL
Management of AGC
Most common route of spread
Most cervical cancers occur in the
Most common type of cervical cancer
associated with DESexposure
Most common symptom of cervical
cancer
Treatment for cervical cancer
Overall five-year survival rate
• Age 65: if with no history ofCIN 11/111/CIS/cervical
cancer, and with prior negative results (Two negative
primary HPVtests, two negative co-tests, or three
negative Pap smears within the last 10 years)
cancer,may
• Ifwith no historyofCIN 11/111/CIS/ceIVical
stop screening after total hysterectomy
• Continue screening for a total of 20 years after
spontaneous regression or treatment of lesions, even
beyond 65 years old
• If 21-24 years old: Repeat Pap smear in 12 months
(preferred), OR reflex HPV testing:
• If negative, return to routine screening
• If positive, repeat cytology in 12 mo
• If;eZS years old: Repeat Pap smear in 1 year
(acceptable) OR HPV testing (preferred):
• lfHPV negative test: Repeat co-testing in 3 years.
• If HPV positive test: Colposcopy and cervical
biopsy if needed
• Colposcopy with cervical biopsies if indicated
• If 21-24 years old: Manage as ASC-USexcept reflex
HPV testing
• If ;e25 years old:
• If HPV unknown: Repeat Pap smear in 1 year
(acceptable) OR HPV testing (preferred):
• If HPV negative: Repeat co-testing in 3 years
• If HPV positive: Colposcopy and cervical biopsy
if needed
• Colposcopy with cervical biopsies if indicated;
immediate LEEP acceptable if ;e25 years old
• If 21-24 years old: Colposcopy with cervical biopsies
if indicated
• If 25 years old: Colposcopy, HPV screen, cervical
biopsies, endocervical sampling
• Endometrial,:jopsy in women ;,35 years old
and in women with risk factors for endometrial
hyperplasia, EIN, and endometrial cancer
• Direct extension
• Transformation zone
• Clear cell adenocarcinoma
• Postcoital bleeding
• Stage !Al - IlA2 - surgery or radiotherapy
• Stage JIB - IV - chemoradiotherapy
• Recurrent disease - chemotherapy
• Palliative - radiotherapy, chemotherapy
• 80-93% for Stage I, 15-16% for Stage IV
555
I
.
ENDOMETRIAL NEOPLASIA
Most common exogenous source of
estrogen leading to EIN
Classical symptom ofEIN and
endometrial cancer
Criteria for endometrial biopsy
Initial treatment for EIN
Definitive management for EIN
Type I endometrial cancer
Type II endometrial cancer
Most common route of spread
Most common type of endometrial cancer
Most important prognostic factor for
endometrial carcinoma
Risk factors for endometrial cancer
Disease entities at risk for endometrial
cancer development
Treatment for endometrial cancer
Overall five-year survival rate
556
• Estrogen hormone replacement without
progesterone
• Postmenopausal bleeding or AUB
• Woman >45 years old with abnormal uterine
bleeding
• Postmenopausal women with abnormal uterine
bleeding, or EM stripe ~4 mm
• Oral medroxyprogesterone acetate or megestrol
acetate
• Hysterectomy
• Occurs in women with history of chronic
unopposed estrogen exposure
• Start as atypical endometrial hyperplasia or EIN
• Endometrioid
• More favorable prognosis
• Non-estrogen dependent
• Start in atrophic endometrium
• Serous or clear cell histology
• Associated with p53 mutations
• Less favorable prognosis
• Direct extension
• Endometrioid adenocarcinoma
• Histologic grade
• Unopposed estrogen stimulation of the
endometrium
• Unopposed menopausal estrogen (4-8x)
replacement therapy
• Menopause after 52 years (2.4x)
• Obesity (2-5x)
• Nulliparity (2-3x)
• Diabetes (2.8x)
• Insulin resistance
• Estrogen secreting ovarian tumors
• Polycystic ovarian syndrome (PCOS)
• Tamoxifen therapy for breast cancer
• Lynch II syndrome, Cowden syndrome, Peutz-
Jeghers syndrome, BRCAmutations
• Mainstay is extra fascia! hysterectomy and
bilateral salpingooophorectomy (EHBSO),pelvic
and para-aortic lymph node dissection
• Add radiotherapy if high risk for Stage 1-11,
chemoradiotherapy for Stage Ill-IV
• Recurrent - chemotherapy± radiotherapy
• 65%
OVARIAN CANCER
Most common cause of gynecologic
cancer death
Reasons for high mortality among
ovarian cancer patients
Most common route of spread
Most common lymph node site
Main etiology of ovarian cancer
Risk factors for ovarian cancer
Eponym for ovarian malignant
metastases to the umbilicus
Primary staging for epithelial ovarian
cancer
Serum marker for epithelial ovarian
cancer monitoring
Treatment of epithelial ovarian cancer
Most common ovarian malignancy in
women <20 years old
Most common germ cell tumor
Most common malignant germ cell tumor
Serum markers for germ cell tumors
Treatment of germ cell tumors
Functional ovarian tumors
Pathognomonic sign for granulosa cell
tumors
Meigs syndrome
Hormones produced by sex-cord stromal
tumors
Treatment of sex cord stromal tumors
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• Ovarian cancer
• Lack of effective screening tools
• Presentation at late stages of the disease
• Peritoneal
• Retroperitoneal pelvicand para-aortic lymph nodes
• STIC,incessant ovulation
• Age
• Diet
• Family history
• Industrialized country
• Infertility
• Nulliparity
• Ovulation and ovulatory drugs
• Talc (controversial)
• Sister Mary Joseph nodule
• Peritoneal fluid cytology, total
abdominal hysterectomy with bilateral
salpingooophorectomy (TAHBSO),
omentectomy, peritoneal biopsy, and pelvic and
para-aortic lymph node dissection
• CA-125
• Surgery ± chemotherapy
• Germ cell tumors
• Benign cystic mature teratoma (dermoid cyst)
• Dysgerminoma
• LDH - dysgerminoma
• AFP - endodermal sinus (yolk sac) tumor,
immature teratoma
• hCG - choriocarcinoma
• Unilateral salpingooophorectomy with complete
surgical staging± multiagent chemotherapy
(surgery only for Stage IA dysgerminoma and
immature teratoma, grade 1)
• Granulosa cell tumor, Sertoli-Leydig cell tumor
• Call-Exner bodies (coffee bean nuclei, with cells
arranged in small clusters around a central cavity)
• Fibroma, ascites, pleural effusion
• Granulosa-theca - estradiol and inhibin
• Sertoli-Leydig - androgens
• Fibroma - none
• Unilateral salpingooophorectomy with complete
surgical staging ± multiagent chemotherapy if
desirous of future pregnancy
• Primary staging (same as that for epithelial
ovarian cancer) if completed family size or
postmenopausal
I
.
GESTATIONAL TROPHOBLASTIC DISEASE (GTD)
• Molar pregnancy (most common)
• Persistent GTD and invasive moles
Four classifications of GTDs
• Gestational choriocarcinoma
• Placental site trophoblastic tumors (PSTI) (rare)
• Extremesin age,prior historyof GTD(most common)
• Nulliparity
• Paternal age > 45 years
Risk factors for molar pregnancy • Diet low in beta-carotene, folic acid, animal fat
• Smoking
• Infertility
• Spontaneous abortion, previousmolarpregnancy
Most common symptom of molar pregnancy • Vaginal bleeding
Racial predilection for GTD • Southeast Asians, particulary Japanese
Pathogenesis ofcomplete molar pregnancy • Fertilization of empty egg
Most common karyotype of complete moles • 46XX
Effects of extreme levels of beta hCGin • Theca lutein cysts, hyperthyroidism,
complete moles hyperemesis gravidarum, preeclampsia
• Snowstorm pattern secondary to widespread
Ultrasound pattern for complete moles
chorionic villi swelling
Pathogenesis of partial molar pregnancy • Fertilization of normal ovum with two sperms
Most common karyotype of partial moles • 69XXY
Partial moles are often misdiagnosed as • Spontaneous or missed abortions
Ultrasound pattern for partial molar • Swiss-cheese appearance secondary to focal
pregnancy hydropic villi
Treatment for molar pregnancy • Suction curettage
• 48 hrs after evacuation, then every 1-2 weeks
Monitoring hCGlevels post-molar
until negative for 3 consecutive weeks, then
pregnancy
monthly for 6 months
• 14 weeks for complete mole
Average hCGnormalization time
• 8 weeks for partial mole
• 1-2% after one molar pregnancy
Risk of recurrent GTD
• 16-32% after two molar pregnancy
Low-risk GTNtreatment • Single-agent chemotherapy
High-risk GTNtreatment • Combination chemotherapy
• hCG >100,000 mlU/mL
Risk factors for persistent postmolar • Uterine size >14-16 weeks
GTDand invasive moles • Theca lutein cysts >6 cm
• Coexistent fetus

Characteristic feature of gestational • Sheets of anaplastic trophoblast without

choriocarcinoma chorionic villi, with necrosis
Primary symptom of gestational
• Late postpartum bleeding
choriocarcinoma
Characteristic feature of PSTTs • Excessive production of human placental lactogen
Primary symptom of PSTTs • Persistent irregular vaginal bleeding
Treatment of choice for PSTTs • Hysterectomy

REFERENCES
I.Callahan T.Caughey A. Blueprints: Obstetrics and Gynecology, 7th Edition. 2018

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